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Book Review: In the Pleasure Groove by John Taylor
I'm going to come clean right away and admit I have a bias in reviewing In The Pleasure Groove by John Taylor. I'm a card-carrying Duranie. Literally, when I was a teen I had packs of those bubble gum trading cards...but I digress. Truth be told, I've been waiting for this book to be released since I first learned about it about six months ago. Having the opportunity to officially review it was exciting.
I'm not worried about any conflict of interest though. There will be many strong literary reviews of the book in every medium known to man. After all, my "D Blast" just informed me this morning that the book debuted in the top 10 in both England and the United States. Considering this, I am content to wax somewhat more philosophical than I ordinarily might.
Being a musician and singing teacher, I feel a distant mentorship with "the Boys" that transcends the hype and idolatry that characterized Duran Duran's existence in the early 80's. Yes, Taylor's honesty in Pleasure Groove does throw the curtain back on my Oz. Still, it is worth diluting the mystery to better understand the ways in which our shared experience from opposite sides of the same cultural phenomenon impacted the people of Duran Duran. Recognition of celebrities' humanity is often lost in the shuffle of photo ops and press junkets. This loss can flay the entertainer and deprives the fan of understanding the source of the works that move them.
In The Pleasure Groove includes many details about Taylor's early life, which is helpful in understanding his later trajectory. Little things like his hatred of his glasses, getting picked last in gym class and the time he spent building models of military vehicles help pull you into a world where it is possible that John Taylor of Duran Duran could have actually been a young boy named Nigel. The mundane circumstances of his upbringing belie the notion that all out-of-control rockers must have been the product of broken and hopelessly dysfunctional homes.
John discovered his visceral connection to music and the possibility of being a professional in 1976 after becoming entranced by The Sex Pistols' "Anarchy in the UK." This is a fun story on the first reading, but it's even better to reread while listening to the song on YouTube. Try it!
This early musical influence may have been a foreshadowing of the challenges he would face interpersonally and with addiction. There are many theoretical debates taking place about the extent to which humanity is truly in possession of free will. While I can't get on board with the utter nihilism of many of these theorists, I believe there are certain pivotal moments in our lives where one set of options falls irrevocably away and others present themselves with little alternative. John Taylor's exposure to "Anarchy in the UK" is one of those moments. If there was any doubt that he would become a successful musician, that possibility died that day.
Having read various brief or unauthorized biographies in my younger years, I thoroughly enjoyed hearing the complete true story of how all of the members of Duran Duran met and coalesced. Evident in Taylor's telling of it is the vast differences in personality and style of each member. With this diversity, you can see how their early decision to share all songwriting credit and make decisions together was crucial to the development of their sound. He is correct in asserting that if any one member had been allowed to dominate, the music would not have been as unique or interesting.
Much of the book is dedicated to discussion of Taylor's struggles with depression and addiction. I'm certain most of the clarity and analysis of his own behavior must have come after the fact. This is the way the human mind works, we experience first and make sense of it later. For a Duranie reading this, it seems as if there were two John Taylors living in alternate dimensions. One was a confident man charming us all from the stage and through MTV. The other was a cringing man who couldn't bear the thought that he might not be all that important after all and whose rage almost cost him the use of his most important picking finger.
I admit it is difficult for me to read about the painful parts of Taylor's musical life. As a fan, I was a part of what was driving him mad. I was one of the screaming masses at the Worcester Centrum on the Seven and the Ragged Tiger tour. Musically and psychologically I took much from them. Yes, it is ultimately a symbiotic relationship between entertainer and fan. It still seems to me that, save for a few psycho stalkers, it is the entertainer who more often breaks down under the strain.
After being treated to such wonderful detail in terms of the hyper-Duran years, Taylor's post-rehab life was somewhat glossed over. His recollections of playing solo on tour to eight people in the audience and playing on the street to people who didn't want to believe it was really him were touching. They also serve to connect us back to what this man really lives for--music. He states later in the book that as long as he still has the calluses on his fingertips and he can still make music, he'll be okay.
The book would have benefitted from more details about the years Taylor spent away from Duran Duran. He refers to making music, I would have loved to understand more about what form that took with his talent freed from the corporate music industry machine. Interestingly, he never mentions (at least by name) his solo album Feelings Are Good and Other Lies. Maybe this is because of the heavy emotional content evident in the songwriting. (The ballad Losing You still makes me cry.) Feelings Are Good was a raw album, both in terms of content and production values. It was clearly an album his soul needed to make, regardless of it's potential commercial market value. As a Duranie reading this book, I crave greater context for that album.
I was privileged to see Taylor at Mama Kin in Boston when he toured with Neurotic Outsiders, but didn't know at the time he was so recently relieved of his demons. What I did know is that it was a phenomenal show. Billy Idol was guesting that night. Standing eight feet from the stage, I felt their energies fill the room in a way that is not quite possible in a large arena. It's the closest I'll ever come to the fabled Rum Runner experience.
After the show, my friend and I actually followed some chick named Vicki around for about an hour to see if we could meet the band. We figured we actually had a shot at it, since she was dressed like she knew how to make such things happen.
As you can tell by now, I'm hopelessly sentimental. I don't know what I expected to say, if presented with an opportunity to meet John Taylor. There was too much to communicate with words. So, in the end all I ended up doing was mumbling "Thank you" as I shook his hand.
Thank you again, John, for this truthful and yet still understated book. I recommend it and eagerly await your next musical contribution to the world.


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Reports are coming in that Chick-Fil-A's Vice President of Corporate Public Relations, Donald Perry, has died of a heart attack this morning.
The restaurant has been hit by progressive backlash after its CEO, Dan Cathy, said he was against same sex marriage in response to a reporter's question.
After the interview went public, progressives threatened to boycott the business and the mayors of Boston and Chicago threatened to ban the businesses from opening locations in their areas.

subset: commoncrawl


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Skipp Pearson Jazz Foundation
"Put a Little Jazz in Your Life"
I-95 Corridor Jazz in Blue Series
(click here to purchase and reserve your seats for this performance)
Skipp Pearson and the men and woman who represent the Skipp Person Jazz Ensemble are heading up and down I-95 taking the unique sound of classic jazz music to cities and town along the corridor.
You can have an evening of live jazz music with Skipp Pearson and Band for a nominal fee. Call and book your evening today at 1.803.400.1879.


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• "Investing in a Period of Uncertainty": 12 Resources for Investors
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WASHINGTON, D.C.//June 27, 2013//The nonprofit Alliance for Investor Education (AIE) is issuing today "Recursos en español sobre ahorros e inversiones/Saving and Investing Resources in Spanish" a round-up of the best available investor education resources in Spanish. AIE is a consortium of 21 leading U.S. financial-related foundations, nonprofit organizations, associations and governmental agencies.
AIE President Sue Duncan, who also serves as vice president of the Investment Company Institute Education Foundation (ICIEF), said: "Many members of the Alliance offer a variety of materials for Spanish-speaking consumers and those who work with and help inform investors. By compiling a number of these top saving and investing resources in one place, we hope to be a one-stop shop for consumers, financial advisers and educators who need the best in saving and investing resources in Spanish."
The new Recursos en español sobre ahorros e inversiones / Saving and Investing Resources in Spanish section of the AIE Web site features the following 10 top resources for consumers:
Ballpark E$timate en español/Ballpark E$timate in Spanish - American Savings Education Council/Employee Benefit Research Institute. This is an easy-to-use, two-page worksheet that helps you quickly identify approximately how much you need to save to fund a comfortable retirement.
Estafas y chantajes: Una guía educativa para prevenir fraudes financieros/Scams and Swindles: An Educational Guide to Avoiding Investment Fraud - National Futures Association. This guide describes common characteristics of investment scams and outlines steps individuals can take to avoid them.
Hágase cargo antes de que una mala inversión se haga cargo de usted / Take Charge Before a Bad Deal Takes You - Investor Protection Trust. This is a brochure about the warning signs of financial fraud and how to do your research to avoid being a victim of fraud.
¡Cuidado, alguien quiere su dinero!/Careful Someone Wants Your Money - U.S. Commodity Futures Trading Commission (CFTC). This includes resources from the CFTC on how to protect yourself from fraud, the warning signs of fraud and different types of fraud.
Cómo invertir en bonos con inteligencia/Smart Bond Investing - Financial Industry Regulatory Authority. This is a guide to help current and future bond investors better understand bonds as an important component of a balanced portfolio.
Declaración de los derechos de los inversionistas/Statement of Investor Rights - CFA Institute. The Statement of Investor Rights was developed by CFA Institute to advise buyers of financial service products of the conduct they are entitled to expect from financial service providers.
Cómo detener el fraude de afinidad en su comunidad/Stopping Affinity Fraud in Your Community - U.S. Securities and Exchange Commission. This guide looks to raise awareness regarding investment scams that target specific groups. It teaches key strategies that investors can use to protect themselves and their community from the potentially devastating impact of affinity fraud.
Sitio web Asuntos de dinero/Money Matters web site - Federal Trade Commission. The Federal Trade Commission (FTC), the nation's consumer protection agency, created this website to help consumers tackle some money issues, like managing your money, looking out for scams, credit cards and dealing with debt, among other things.
Sitio web de Hispanic America Saves/Hispanic America Saves website - supported by The Investment Company Institute and FINRA Education Foundation, among others. America Saves is a campaign dedicated to helping consumers save money, reduce debt and build wealth.
Sitio web en español de SIPC/SIPC website - Securities Investor Protection Corporation. This is the website for the Securities Investor Protection Corporation, the U.S. investor's first line of defense in the event of the failure of a brokerage firm owing customers cash and securities that are missing from customer accounts.
For an overview of the rest of the best investor education resources on the Web from AIE members, go to http://www.investoreducation.org.
Founded in 1996, the Alliance for Investor Education Web site at http://www.investoreducation.org provides investors with access to a full range of information they need to make wise investment decisions. The 22-member Alliance for Investor Education is dedicated to facilitating greater understanding of investing, investments and the financial markets among current and prospective investors of all ages. We pursue initiatives for education and join with others to motivate Americans to obtain objective information and increase their knowledge and understanding of investing.
Full members of the Alliance include: American Association of Individual Investors, American Institute of Certified Public Accountants/360 Degrees of Financial Literacy, CFA Institute, Certified Financial Planner Board of Standards, Inc., Employee Benefit Research Institute/American Savings Education Council, Financial Industry Regulatory Authority, Investment Company Institute Education Foundation, Investor Protection Trust, Insured Retirement Institute, National Association of Real Estate Investment Trusts, National Endowment for Financial Education, National Futures Association, Options Industry Council, SIFMA Foundation, Securities Investor Protection Corporation, and the Society for Financial Education and Professional Development.
The U.S. Securities and Exchange Commission, U.S. Commodity Futures Trading Commission, the U.S. Federal Trade Commission's Bureau of Consumer Protection, the Board of Governors of the Federal Reserve System, and the North American Securities Administrators Association are the governmental and quasi-governmental advisors to the Alliance.
CONTACT: Ailis Aaron Wolf, for AIE, (703) 276-3265 or firstname.lastname@example.com.
Bond Price Tables
Bond Yield Calculator
Buying And Selling Bonds
Callable and Redeemable Bonds
Guide to Bond Basics
High-Yield Bonds
Municipal Bonds
Reading Bond Prices
Smart Bond Investing
What Are Bonds?
Why Bond Prices Go Up and Down
401(k) Plans
401(k) Resource Center
An Investor's Checklist for Selecting a Professional Financial Advisor
Ballpark E$timate
Consumer Guide to financial Planning
FAQ on 529s
Free Credit Reports
Fundamentals of Saving and Investing
Get Smart About Your Money
Intro to 529 Plans
Managing The Relationship Between You and Your Advisor
MoneyTrack TV series
Roth Vs. Traditional IRAs
Social Media and Investing
Women and Pensions - What Women Need to Know and Do
An Online Learning Guide to Trading Futures
A Guide to the Language of the Futures Industry
Background Affiliation Status Information Center (BASIC)
Basics of Futures Trading
Forex Fraud Warning
Forex Online Learning Program
Forex: What Investors Need To Know
Single Stock Futures
Arbitration and Mediation
ID Theft
Katrina Victims
SIPC Claims
State Securities Agencies
What is a CFA Charterholder?
12 Common Investor Errors
Ahorrando para el futuro
Annuities (NASD)
Asset Allocation
Defining Investment Objectives
Investor 'Survival Skills' Lacking
MoneyTrack TV series
Opening a Brokerage Account
Researching Investments
Saving for Retirement
Tomorrow's Money
A Guide For Investors
Closed End Funds
Figuring out Your Mutual Fund Portfolio
Mutual Fund Breakpoints
Mutual Fund Expense Analyzer
Mutual Fund Fees
Socially Responsible Mutual Funds
Avoiding Investment Fraud and Abuse
Investing Basics for Older Americans
Its Never Too Late To Save
Planning for Stages of Retirement
Reaching Retirement Goals
Retirement Catch-up for Late Starters
Retirement Myths
Senior Investment Resources
Threats to Senior Investors
Top Ten Ways To Beat The Clock And Prepare For Retirement
What To Know About 'Senior Specialists'
Consumer Guide to Financial Self-Defense
Cross-border Online Fraud
Dont Become a Victim of Investment Fraud
Elder Investment Fraud
Know the Signs of Fraud
Opportunities & Risks
Phantom Regulators
Poaching Veterans Pensions
Protecting Online Brokerage Accounts
Pump-and-Dump Schemes
Scams and Swindles
Social Networking Fraud
Top 10 Scams
What You Can Do to Avoid Investment Fraud
Analyzing Analyst Recommendations
EDGAR Filings
Hedge Funds: Are They Right for You?
Securities Regulation
What is a hedge fund?
What Steps You Should Take When Your Stock's Price Falls
Economic History in the U.S.
Financial Workshop Kits
For Students
Fraud Scene Investigator
NEFE High School Financial Planning Program
NYSE Teacher Workshop
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Building Wealth
For Students
Fraud Scene Investigator
Just Starting Out
Kid's Savings Calculator
Kid's Savings Game


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House speaker defends choice of Rush Limbaugh for induction into Hall of Famous Missourians
JEFFERSON CITY, Mo. (AP) ' While advertisers flee his radio show, conservative talk show host Rush Limbaugh is poised to be added to the Hall of Famous Missourians in the state Capitol.
Inductees are chosen by the speaker of the Missouri House. Speaker Steven Tilley said Monday he decided to honor Limbaugh months ago. The Republican lawmaker and Limbaugh are both from the state's southeastern corner.
Limbaugh's show has lost nine advertisers since he referred last week to a female law student involved in the national debate about insurance for contraception as a "slut" and "prostitute." Limbaugh has since apologized.
Tilley is defending his choice, saying Limbaugh is among the world's best-known radio personalities. Tilley also says the hall honors famous Missourians ' not "universally loved Missourians."


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When I came home from playing football today I took a shower. About two minutes in, my eye caught sight of a small black shape moving very organically at my feet. When I reached down to touch it, the water splashed over my back, changed its course and the particle lost its wobble. I realised that it was just a piece of dirt that had made the trip home from the pitch with me. Haven't you shared similar experiences? seen a piece of matter moved by the elements, wind or water, in such a way that it appears alive? It exists as alive in our mind until our perception receives additional information to think otherwise. Yet the same elements are inside of us and every living being, and the consensus is that there they're very incontestably driving life.
One of the first concepts we are taught upon beginning high-school biology is that everything on Earth exists in at least one of four planetary layers: the lithosphere, the hydrosphere, the atmosphere and the biosphere (solid minerals, water, air and life). We accept that chemical reactions define the processes in each one, but in the biosphere these chemical cycles operate in tandem with the unique force of life that imbues them and as such are considered to be in a class of their own. This attribute makes the biosphere distinct, but from an outside perspective, life can also be seen as just another set of organizational forces that determine how matter comes to be structured. Life is a continuation of the energy that blew apart and created all the elements that surround us long ago, and that continues to propagate to create evermore diverse and chaotic mixed structures. Humans have invented communication networks that allow even ideational flows to participate in structuring these material flows (and viceversa), but we're not the only species that is moved to transform through ideas. When sea birds congregate in the millions on islands in the middle of the ocean to find a mate and have offspring, they surely also tell each other something about the world during the months that they spend next to each other on a barren rock. When they leave, this collectively propagated information influences how they act upon their environment.
To me life is perplexing and wonderful because it appears to have its own unique dynamics while simultaneously following the elemental properties of its constituent matter. How much of how we move, think, feel and express do you think is actually due to the fact that we are mostly made up of water?


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One more way to eliminate the amount of waste coming into your home and going out to the landfill or recycling facility.
For four bags you will need one yard of tulle and 8 yards of ribbon.
These are super simple to make if you can sew a straight line.
I used tulle to keep them as lightweight and easy to clean as possible.
The yard of tulle that I purchased was 56 inches wide. I cut it into four pieces that were 18 inches by 28 inches to maximize the full yard of tulle.
Turn the long sides up about a 1/2 inch and stitch.
Turn the short sides up about 3/4 of an inch inch toward the same side of the fabric as you did the sides and stitch. This will make the casing for the drawstrings.
The side of the fabric that you turned those edges to is the WRONG side.
Fold the piece in half, with RIGHT sides together, so that the two short ends meet up. Stitch up the sides starting BELOW the casings you made previously and down to the folded edge. You need that casing to remain open to thread the drawstring through.
Repeat on the other side, exactly the same way.
Now turn your bag right side out.
Slip a safety pin onto the end of one yard of ribbon and thread it through one side of the casing and into the other, coming back out where you started.
Tie those ends together in a knot.
Attach the safety pin to another yard of ribbon and feed it into the casing on the opposite side as before. Take it through the casing on one side and into the other, coming back out where you started again. Tie the ends together in a knot.
This makes the drawstrings cinchable.
That's it! You're done!
I made four bags in just under an hour. I spent only $1 on the yard of tulle. I had the ribbon and thread on hand.
Here are the comparisons between the plastic and reusable bags.
The plastic bag from the grocery store weighs 1/10th of an ounce.
The reusable bag weighs 2/10ths of an ounce.
My scale is pretty sensitive and couldn't decide between .1 and .2.
I snapped the picture at .2.
When fully opened, the size of the plastic bag is about 14 inches by 14 inches.
The reusable bag is about 13 inches by 16 inches.
Plastic bag: Can possibly be reused once or twice. Then it goes in the garbage. OR to the recycling bin where it will go to a recycling facility which may or may not be in the U.S. and will consume energy in the recycling process.
Reusable bag: Keep it and use it over and over again.
Tulle can be machine washed and tumble dried on low according to the care label on the bolt of fabric.
I think it would be just as easy to wash the bags in a sink full of soapy water, rinse, and air dry. Which won't take long at all for the tulle.
Some of my reusable grocery bags have a zippered pocket inside them. I've never had a use for that pocket but now I think it will be the perfect place to store my produce bags until I need them in the store. 🙂
Pin It


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Chris L Jones is a freelance food, garden, lifestyle and travel photographer. He is based at CI Studios in Erskineville, Sydney Australia, where he works in the studio and on location.
The studio has various large spaces including cycs, kitchens and areas suitable for daylight work. It is fully digital and support staff are available on request including producers, retouchers,assistants etc. there is also an affiliated studio in Melbourne.
After assisting top photographers in London and Paris he emigrated to Australia and has worked for many different editorial, advertising, design and publishing clients.
Among the many books he has contributed to areThe Food of France and Food of Italy (Murdoch Books) as well as Girlosophy (Allen and Unwin) and Balcony (Lothian). He also sells work direct from his extensive picture library which specialises in garden and travel photography.


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Articles by Deanna P. Bracy
Other Publications (23)
- American Journal of Physiology. Endocrinology and Metabolism
- American Journal of Physiology. Endocrinology and Metabolism
- The Journal of Nutrition
- American Journal of Physiology. Endocrinology and Metabolism
- Diabetes
- Diabetes
- American Journal of Physiology. Endocrinology and Metabolism
- Endocrinology
- The Journal of Biological Chemistry
- American Journal of Physiology. Endocrinology and Metabolism
- The Journal of Physiology
- The Journal of Physiology
- Diabetes
- Diabetes
- Diabetes
- The Journal of Physiology
- Diabetes
- Diabetes
- Biochimica Et Biophysica Acta
- Endocrinology
- The Journal of Biological Chemistry
- American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
- Endocrinology
Articles by Deanna P. Bracy in JoVE
Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice Julio E. Ayala1, Deanna P. Bracy2,3, Carlo Malabanan3, Freyja D. James2,3, Tasneem Ansari3, Patrick T. Fueger4, Owen P. McGuinness2,3, David H. Wasserman2,3 1Diabetes and Obesity Research Center, Sanford-Burnham Medical Research Institute at Lake Nona, 2Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, 3Vanderbilt Mouse Metabolic Phenotyping Center, Vanderbilt University School of Medicine, 4Department of Pediatrics and Cellular and Integrative Physiology, Indiana University School of Medicine The hyperinsulinemic-euglycemic clamp, or insulin clamp, is the gold standard for assessing insulin action in vivo. A method for performing insulin clamps in mice is described. This includes a method for arterial catheterization that permits experiments to be performed in conscious, unrestrained mice with minimal stress.
Other articles by Deanna P. Bracy on PubMed
Fiber Type-specific Determinants of Vmax for Insulin-stimulated Muscle Glucose Uptake in Vivo American Journal of Physiology. Endocrinology and Metabolism. Mar, 2003 | Pubmed ID: 12556351 The aim of this study was to determine barriers limiting muscle glucose uptake (MGU) during increased glucose flux created by raising blood glucose in the presence of fixed insulin. The determinants of the maximal velocity (V(max)) of MGU in muscles of different fiber types were defined. Conscious rats were studied during a 4 mU x kg(-1) x min(-1) insulin clamp with plasma glucose at 2.5, 5.5, and 8.5 mM. [U-(14)C]mannitol and 3-O-methyl-[(3)H]glucose ([(3)H]MG) were infused to steady-state levels (t = -180 to 0 min). These isotope infusions were continued from 0 to 40 min with the addition of a 2-deoxy-[(3)H]glucose ([(3)H]DG) infusion. Muscles were excised at t = 40 min. Glucose metabolic index (R(g)) was calculated from muscle-phosphorylated [(3)H]DG. [U-(14)C]mannitol was used to determine extracellular (EC) H(2)O. Glucose at the outer ([G](om)) and inner ([G](im)) sarcolemmal surfaces was determined by the ratio of [(3)H]MG in intracellular to EC H(2)O and muscle glucose. R(g) was comparable at the two higher glucose concentrations, suggesting that rates of uptake near V(max) were reached. In summary, by defining the relationship of arterial glucose to [G](om) and [G](im) in the presence of fixed hyperinsulinemia, it is concluded that 1) V(max) for MGU is limited by extracellular and intracellular barriers in type I fibers, as the sarcolemma is freely permeable to glucose; 2) V(max) is limited in muscles with predominantly type IIb fibers by extracellular resistance and transport resistance; and 3) limits to R(g) are determined by resistance at multiple steps and are better defined by distributed control rather than by a single rate-limiting step.
Hexokinase II Partial Knockout Impairs Exercise-stimulated Glucose Uptake in Oxidative Muscles of Mice American Journal of Physiology. Endocrinology and Metabolism. Nov, 2003 | Pubmed ID: 12865258 Muscle glucose uptake (MGU) is distributively controlled by three serial steps: delivery of glucose to the muscle membrane, transport across the muscle membrane, and intracellular phosphorylation to glucose 6-phosphate by hexokinase (HK). During states of high glucose fluxes such as moderate exercise, the HK activity is of increased importance, since augmented muscle perfusion increases glucose delivery, and increased GLUT4 at the cell membrane increases glucose transport. Because HK II overexpression augments exercise-stimulated MGU, it was hypothesized that a reduction in HK II activity would impair exercise-stimulated MGU and that the magnitude of this impairment would be greatest in tissues with the largest glucose requirement. To this end, mice with a HK II partial knockout (HK+/-) were compared with their wild-type control (WT) littermates during either sedentary or moderate exercise periods. Rg, an index of glucose metabolism, was measured using 2-deoxy-[3H]glucose. No differences in glucose metabolism were detected between sedentary groups. The increase in Rg due to exercise was impaired in the highly oxidative heart and soleus muscles of HK+/- compared with WT mice (7 +/- 10 vs. 29 +/- 9 and 8 +/- 3 vs. 25 +/- 7 micromol. 100 g-1. min-1, respectively). However, the increase in Rg due to exercise was not altered in gastrocnemius and superficial vastus lateralis muscles in HK+/- and WT mice (8 +/- 2 vs. 12 +/- 3 and 5 +/- 2 vs. 8 +/- 2 micromol. 100 g-1. min-1, respectively). In conclusion, MGU is impaired by reductions in HK activity during exercise, a physiological condition characterized by high glucose flux. This impairment is critically dependent on the tissue's glucose metabolic rate and correlates with tissue oxidative capacity.
Quinides of Roasted Coffee Enhance Insulin Action in Conscious Rats The Journal of Nutrition. Nov, 2003 | Pubmed ID: 14608069 Consumption of large amounts of coffee has been shown to decrease the incidence of type 2 diabetes. However, the specific compounds and mechanisms responsible for this effect are not known. The aim of this study was to determine the effects of a decaffeinated coffee extract and a synthetic quinide, representative of those found in roasted coffee, 3,4-diferuloyl-1,5-quinolactone, on insulin-stimulated glucose disposal and muscle glucose uptake. Experiments were performed on conscious rats during hyperinsulinemic, euglycemic clamps receiving gastric infusions of saline, a decaffeinated coffee extract (DECAF) (220 mg/kg), or 3,4-diferuloyl-1,5-quinide (DIFEQ) (110 mg/kg). Following treatment, rats received an intravenous bolus of deoxy-[2-3H] glucose to assess muscle glucose uptake (Rg, micromol x 100 g(-1) x min(-1)). Glucose infusions [mg/(kg x min)] required to maintain euglycemia during the tracer period were higher with DIFEQ (14.6 +/- 0.7) than with saline (10.8 +/- 0.7) and DECAF (11.5 +/- 1.1). Despite increased glucose requirements, Rg in skeletal (soleus, gastrocnemius, superficial vastus lateralis) and cardiac muscle were unchanged. DECAF or DIFEQ did not affect heart rate, blood pressure, plasma nonesterified fatty acids or liver aminotransferase activity. These results demonstrate that DIFEQ increases whole-body glucose disposal independently of skeletal muscle Rg.
Distributed Control of Glucose Uptake by Working Muscles of Conscious Mice: Roles of Transport and Phosphorylation American Journal of Physiology. Endocrinology and Metabolism. Jan, 2004 | Pubmed ID: 13129858 Muscle glucose uptake (MGU) is determined by glucose delivery, transport, and phosphorylation. C57Bl/6J mice overexpressing GLUT4, hexokinase II (HK II), or both were used to determine the barriers to MGU. A carotid artery and jugular vein were catheterized for arterial blood sampling and venous infusions. Experiments were conducted in conscious mice approximately 7 days after surgery. 2-Deoxy-[3H]glucose was administered during rest or treadmill exercise to calculate glucose concentration-dependent (Rg) and -independent (Kg) indexes of MGU. Compared with wild-type controls, GLUT4-overexpressing mice had lowered fasting glycemia (165 +/- 6 vs. 115 +/- 6 mg/dl) and increased Rg by 230 and 166% in the gastrocnemius and superficial vastus lateralis (SVL) muscles under sedentary conditions. GLUT4 overexpression was not able to augment exercise-stimulated Rg or Kg. Whereas HK II overexpression had no effect on fasting glycemia (170 +/- 6 mg/dl) or sedentary Rg, it increased exercise-stimulated Rg by 82, 60, and 169% in soleus, gastrocnemius, and SVL muscles, respectively. Combined GLUT4 and HK II overexpression lowered fasting glycemia (106 +/- 6 mg/dl), increased nonesterified fatty acids, and increased sedentary Rg. Combined GLUT4 and HK II overexpression did not enhance exercise-stimulated Rg compared with HK II-overexpressing mice because of the reduced glucose concentration. GLUT4 combined with HK II overexpression resulted in a marked increase in exercise-stimulated Kg. In conclusion, control of MGU shifts from membrane transport at rest to phosphorylation during exercise. Glucose transport is not normally a significant barrier during exercise. However, when the phosphorylation barrier is lowered by HK II overexpression, glucose transport becomes a key site of control for regulating MGU during exercise.
Hexokinase II Overexpression Improves Exercise-stimulated but Not Insulin-stimulated Muscle Glucose Uptake in High-fat-fed C57BL/6J Mice Diabetes. Feb, 2004 | Pubmed ID: 14747279 The aim of the present study was to determine the specific sites of impairment to muscle glucose uptake (MGU) in the insulin-resistant high-fat-fed, conscious C57BL/6J mouse. Wild type (WT) and hexokinase II overexpressing (HK(Tg)) mice were fed either a standard diet or high-fat diet and studied at 4 months of age. A carotid artery and jugular veins had catheters chronically implanted for sampling and infusions, respectively, and mice were allowed to recovery for at least 5 days. Mice were fasted for 5 h and underwent a hyperinsulinemic-euglycemic clamp or saline infusion for 120 min. Separate groups of mice were studied during 30-min sedentary or treadmill exercise periods. A bolus of 2-deoxy[(3)H]glucose was administered 25 min before the end of each study for determination of R(g), an index of tissue-specific glucose uptake. Fasting blood glucose was increased in high-fat compared with standard diet-fed WT (194 +/- 4 vs. 171 +/- 4 mg/dl) but not HK(Tg) (179 +/- 5 vs. 171 +/- 3 mg/dl) mice. High-fat feeding created hyperinsulinemia in both WT and HK(Tg) mice (58 +/- 8 and 77 +/- 15 micro U/ml) compared with standard diet-fed mice (21 +/- 2 and 20 +/- 1 micro U/ml). R(g) was not affected by genotype or diet during either saline infusion or sedentary conditions. HK II overexpression augmented insulin-stimulated R(g) in standard diet-fed but not high-fat-fed mice. Exercise-stimulated R(g) was impaired by high-fat feeding in WT mice, but this impairment was largely rectified in HK(Tg) mice. In conclusion, high-fat feeding impairs both insulin- and exercise-stimulated MGU, but only exercise-stimulated MGU was corrected by HK II overexpression.
AMP Kinase-induced Skeletal Muscle Glucose but Not Long-chain Fatty Acid Uptake is Dependent on Nitric Oxide Diabetes. Jun, 2004 | Pubmed ID: 15161745 The purpose of this study was to examine the effects of AMP kinase (AMPK) activation on in vivo glucose and long-chain fatty acid (LCFA) uptake in skeletal muscle and to examine the nitric oxide (NO) dependence of any putative effects. Catheters were chronically implanted in the carotid artery and jugular vein of male Sprague-Dawley rats. After 4 days of recovery, rats were given either water or water containing 1 mg/ml nitro-l-arginine methylester (l-NAME) for 2.5 days. After an overnight fast, rats underwent one of five protocols: saline, 5-aminoimidazole-4-carboxamide-1-B-d-ribofuranoside (AICAR) (10 mg. kg(-1). min(-1)), l-NAME, AICAR + l-NAME, or AICAR + Intralipid (20%, 0.02 ml. kg(-1). min(-1)). Glucose was clamped at approximately 6.5 mmol/l in all groups, and an intravenous bolus of 2-deoxy[(3)H]glucose and [(125)I]-15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid was administered to obtain indexes of glucose (K(g)) and LCFA (K(f)) uptake and clearance. At 150 min, soleus, gastrocnemius, and superficial vastus lateralis were excised for tracer determination. Both K(g) and K(f) increased with AICAR in all muscles studied. K(g) decreased with increasing muscle composition of type 1 slow-twitch fibers, whereas K(f) increased. In addition, AICAR-induced increases in K(g) but not K(f) were abolished by l-NAME in the majority of muscles examined. This shows that the mechanisms by which AMPK stimulates glucose and LCFA uptake are distinct.
AMPK Stimulation Increases LCFA but Not Glucose Clearance in Cardiac Muscle in Vivo American Journal of Physiology. Endocrinology and Metabolism. Nov, 2004 | Pubmed ID: 15265760 AMP-activated protein kinase (AMPK) independently increases glucose and long-chain fatty acid (LCFA) utilization in isolated cardiac muscle preparations. Recent studies indicate this may be due to AMPK-induced phosphorylation and activation of nitric oxide synthase (NOS). Given this, the aim of the present study was to assess the effects of AMPK stimulation by 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR; 10 mg.kg(-1).min(-1)) on glucose and LCFA utilization in cardiac muscle and to determine the NOS dependence of any observed effects. Catheters were chronically implanted in a carotid artery and jugular vein of Sprague-Dawley rats. After 4 days of recovery, conscious, unrestrained rats were given either water or water containing 1 mg/ml nitro-L-arginine methyl ester (L-NAME) for 2.5 days. After an overnight fast, rats underwent one of four protocols: saline, AICAR, AICAR + L-NAME, or AICAR + Intralipid (20%, 0.02 ml.kg(-1).min(-1)). Glucose was clamped at approximately 6.5 mM in all groups, and an intravenous bolus of 2-deoxy-[(3)H]glucose and [(125)I]-15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid was administered to obtain indexes of glucose and LCFA uptake and clearance. Despite AMPK activation, as evidenced by acetyl-CoA carboxylase (Ser(221)) and AMPK phosphorylation (Thr(172)), AICAR increased cardiac LCFA but not glucose clearance. L-NAME + AICAR established that this effect was not due to NOS activation, and AICAR + Intralipid showed that increased cardiac LCFA clearance was not LCFA-concentration dependent. These results demonstrate that, in vivo, AMPK stimulation increases LCFA but not glucose clearance by a NOS-independent mechanism.
Regulation of Insulin-stimulated Muscle Glucose Uptake in the Conscious Mouse: Role of Glucose Transport is Dependent on Glucose Phosphorylation Capacity Endocrinology. Nov, 2004 | Pubmed ID: 15284204 Previous work suggests that normal GLUT4 content is sufficient for increases in muscle glucose uptake (MGU) during hyperinsulinemia, because glucose phosphorylation is the more formidable barrier to insulin-stimulated MGU. It was hypothesized that a partial ablation of GLUT4 would not impair insulin-stimulated MGU when glucose phosphorylation capacity is normal but would do so when glucose phosphorylation capacity is increased. Thus, chow-fed C57BL/6J mice with a GLUT4 partial knockout (GLUT4(+/-)), hexokinase II overexpression (HK(Tg)), or both (HK(Tg) + GLUT4(+/-)) and wild-type littermates were studied. Carotid artery and jugular vein catheters were implanted for sampling and infusions at 4 months of age. After a 5-d recovery, 5-h fasted mice (n = 8-11/group) underwent a 120-min saline infusion or insulin clamp (4 mU/kg.min insulin with glucose maintained at 165 mg/dl) and received a 2-deoxy[(3)H]glucose bolus to provide an index of MGU (R(g)) for the soleus, gastrocnemius, and superficial vastus lateralis. Basal R(g) from all muscles studied from saline-infused mice were not changed by any of the genetic modifications. HK(Tg) mice had augmented insulin-stimulated R(g) in all muscles studied compared with remaining genotypes. Insulin-stimulated R(g) was not impaired in any of the muscles studied from GLUT4(+/-) mice. However, the enhanced insulin-stimulated R(g) created by HK overexpression was ablated in HK(Tg) + GLUT4(+/-) mice. Thus, a 50% reduction of normal GLUT4 content in the presence of normal HK activity does not impair insulin-stimulated MGU. However, when the glucose phosphorylation barrier is lowered by HK overexpression, GLUT4 availability becomes a limitation to insulin-stimulated MGU.
Control of Exercise-stimulated Muscle Glucose Uptake by GLUT4 is Dependent on Glucose Phosphorylation Capacity in the Conscious Mouse The Journal of Biological Chemistry. Dec, 2004 | Pubmed ID: 15456776 Previous work suggests that normal GLUT4 content is sufficient for increases in muscle glucose uptake (MGU) during exercise because GLUT4 overexpression does not increase exercise-stimulated MGU. Instead of glucose transport, glucose phosphorylation is a primary limitation of exercise-stimulated MGU. It was hypothesized that a partial ablation of GLUT4 would not impair exercise-stimulated MGU when glucose phosphorylation capacity is normal but would do so when glucose phosphorylation capacity was increased. Thus, C57BL/6J mice with hexokinase II (HKII) overexpression (HK(Tg)), a GLUT4 partial knock-out (G4(+/-)), or both (HK(Tg) + G4(+/-)) and wild-type (WT) littermates were implanted with carotid artery and jugular vein catheters for sampling and infusions at 4 months of age. After a 7-day recovery, 5-h fasted mice remained sedentary or ran on a treadmill at 0.6 mph for 30 min (n = 9-12 per group) and received a bolus of 2-deoxy[3H]glucose to provide an index of MGU (Rg). Arterial blood glucose and plasma insulin concentrations were similar in WT, G4(+/-), HKTg, and HKTg + G4(+/-) mice. Sedentary Rg values were the same in all genotypes in all muscles studied, confirming that glucose transport is a significant barrier to basal glucose uptake. Gastrocnemius and soleus Rg were greater in exercising compared with sedentary mice in all genotypes. During exercise, G4(+/-) mice had a marked increase in blood glucose that was corrected by the addition of HK II overexpression. Exercise Rg (micromol/100g/min) was not different between WT and G4(+/-) mice in the gastrocnemius (24 +/- 5 versus 21 +/- 2) or the soleus (54 +/- 6 versus 70 +/- 7). In contrast, the enhanced exercise Rg observed in HKTg mice compared with that in WT mice was absent in HKTg + G4(+/-) mice in both the gastrocnemius (39 +/- 7 versus 22 +/- 6) and the soleus (98 +/- 13 versus 65 +/- 13). Thus, glucose transport is not a significant barrier to exercise-stimulated MGU despite a 50% reduction in GLUT4 content when glucose phosphorylation capacity is normal. However, when glucose phosphorylation capacity is increased by HK II overexpression, GLUT4 availability becomes a marked limitation to exercise-stimulated MGU.
Heart-type Fatty Acid-binding Protein Reciprocally Regulates Glucose and Fatty Acid Utilization During Exercise American Journal of Physiology. Endocrinology and Metabolism. Feb, 2005 | Pubmed ID: 15454399 The role of heart-type cytosolic fatty acid-binding protein (H-FABP) in mediating whole body and muscle-specific long-chain fatty acid (LCFA) and glucose utilization was examined using exercise as a phenotyping tool. Catheters were chronically implanted in a carotid artery and jugular vein of wild-type (WT, n = 8), heterozygous (H-FABP(+/-), n = 8), and null (H-FABP(-/-), n = 7) chow-fed C57BL/6J mice, and mice were allowed to recover for 7 days. After a 5-h fast, conscious, unrestrained mice were studied during 30 min of treadmill exercise (0.6 mph). A bolus of [(125)I]-15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid and 2-deoxy-[(3)H]glucose was administered to obtain rates of whole body metabolic clearance (MCR) and indexes of muscle LCFA (R(f)) and glucose (R(g)) utilization. Fasting, nonesterified fatty acids (mM) were elevated in H-FABP(-/-) mice (2.2 +/- 0.9 vs. 1.3 +/- 0.1 and 1.3 +/- 0.2 for WT and H-FABP(+/-)). During exercise, blood glucose (mM) increased in WT (11.7 +/- 0.8) and H-FABP(+/-) (12.6 +/- 0.9) mice, whereas H-FABP(-/-) mice developed overt hypoglycemia (4.8 +/- 0.8). Examination of tissue-specific and whole body glucose and LCFA utilization demonstrated a dependency on H-FABP with exercise in all tissues examined. Reductions in H-FABP led to decreasing exercise-stimulated R(f) and increasing R(g) with the most pronounced effects in heart and soleus muscle. Similar results were seen for MCR with decreasing LCFA and increasing glucose clearance with declining levels of H-FABP. These results show that, in vivo, H-FABP has reciprocal effects on glucose and LCFA utilization and whole body fuel homeostasis when metabolic demands are elevated by exercise.
Control of Muscle Glucose Uptake: Test of the Rate-limiting Step Paradigm in Conscious, Unrestrained Mice The Journal of Physiology. Feb, 2005 | Pubmed ID: 15576451 The aim of this study was to test whether in fact glucose transport is rate-limiting in control of muscle glucose uptake (MGU) under physiological hyperinsulinaemic conditions in the conscious, unrestrained mouse. C57Bl/6J mice overexpressing GLUT4 (GLUT4(Tg)), hexokinase II (HK(Tg)), or both (GLUT4(Tg) + HK(Tg)), were compared to wild-type (WT) littermates. Catheters were implanted into a carotid artery and jugular vein for sampling and infusions at 4 month of age. After a 5-day recovery period, conscious mice underwent one of two protocols (n = 8-14/group) after a 5-h fast. Saline or insulin (4 mU kg(-1) min(-1)) was infused for 120 min. All mice received a bolus of 2-deoxy[(3)H]glucose (2-(3)HDG) at 95 min. Glucose was clamped at approximately 165 mg dl(-1) during insulin infusion and insulin levels reached approximately 80 microU ml(-1). The rate of disappearance of 2-(3)HDG from the blood provided an index of whole body glucose clearance. Gastrocnemius, superficial vastus lateralis and soleus muscles were excised at 120 min to determine 2-(3)HDG-6-phosphate levels and calculate an index of MGU (R(g)). Results show that whole body and tissue-specific indices of glucose utilization were: (1) augmented by GLUT4 overexpression, but not HKII overexpression, in the basal state; (2) enhanced by HKII overexpression in the presence of physiological hyperinsulinaemia; and (3) largely unaffected by GLUT4 overexpression during insulin clamps whether alone or combined with HKII overexpression. Therefore, while glucose transport is the primary barrier to MGU under basal conditions, glucose phosphorylation becomes a more important barrier during physiological hyperinsulinaemia in all muscles. The control of MGU is distributed rather than confined to a single rate-limiting step such as glucose transport as glucose transport and phosphorylation can both become barriers to skeletal muscle glucose influx.
Hexokinase II Protein Content is a Determinant of Exercise Endurance Capacity in the Mouse The Journal of Physiology. Jul, 2005 | Pubmed ID: 15878951 Hexokinase (HK) II content is elevated in fatigue resistant muscle fibres and exercise trained muscle. The aim of this study was to determine if exercise capacity is dependent on muscle HK protein content. C57Bl/6 mice with a 50% HK knockout (HK+/-), no genetic manipulation (wild-type, WT) and an approximately 3-fold HK overexpression (HKTg) were tested. Mice (n = 12/group) completed both a maximal oxygen consumption test(VO2max) test and an endurance capacity test (run at approximately 75% VO2max) on an enclosed treadmill equipped to measure gas exchange. Arterial and venous catheters were surgically implanted into separate groups of mice (n = 9-11/group) in order to measure an index of muscle glucose uptake Rg during 30 min of treadmill exercise. Maximum work rate (0.95 +/- 0.05, 1.00 +/- 0.04 and 1.06 +/- 0.07 kg m min-1), (137 +/- 3, 141 +/- 4 and 141 +/- 5 ml kg-1 min-1) and maximal respiratory exchange ratio (1.04 +/- 0.02, 1.00 +/- 0.03 and 1.04 +/- 0.04) were similar in HK+/-, WT and HKTg, respectively. Exercise endurance capacity (measured as time to exhaustion) increased as HK content increased (55 +/- 11, 77 +/- 5 and 98 +/- 9 min) and this was related to Rg measured in mice during 30 min of exercise (13 +/- 2, 24 +/- 5 and 42 +/- 5 micromol (100 g)-1 min-1). Muscle glycogen in sedentary HK+/-mice and HK+/- mice following 30 min of exercise were significantly lower than in HKTg and WT mice. However, the net exercise-induced muscle glycogen breakdown was equal in the three genotypes. In summary, HK protein content within the range studied (a) was not associated with a difference in the capacity to perform maximal intensity exercise, (b) was a powerful determinant of the ability to sustain moderate intensity exercise, as reducing HK content impaired endurance and increasing HK content enhanced endurance, and (c) although directly related to exercise endurance, was not a determinant of net muscle glycogen usage during exercise. In conclusion, adaptations that increase HK protein content and/or functional activity such as regular exercise contribute to increased muscular endurance.
Partial Gene Deletion of Heart-type Fatty Acid-binding Protein Limits the Severity of Dietary-induced Insulin Resistance Diabetes. Nov, 2005 | Pubmed ID: 16249436 The aim of this study was to determine the contribution of heart-type fatty acid-binding protein (H-FABP) to glucose and long-chain fatty acid (LCFA) utilization in dietary-induced insulin resistance. We tested the hypothesis that H-FABP facilitates increases in LCFA flux present in glucose-intolerant states and that a partial reduction in the amount of this protein would compensate for all or part of the impairment. Transgenic H-FABP heterozygotes (HET) and wild-type (WT) littermates were studied following chow diet (CHD) or high-fat diet (HFD) for 12 weeks. Catheters were surgically implanted in the carotid artery and jugular vein for sampling and infusions, respectively. Following 5 days of recovery, mice received either a saline infusion or underwent a euglycemic insulin clamp (4 mU x kg(-1) x min(-1)) for 120 min. At 90 min, a bolus of 2-deoxyglucose and [125I]-15-(rho-iodophenyl)-3-R,S-methylpentadecanoic acid were administered to obtain indexes of glucose and LCFA utilization. At 120 min, skeletal muscles were excised for tracer determination. All HFD mice were obese and hyperinsulinemic; however, only HFD-WT mice were hyperglycemic. Glucose infusion rates during insulin clamps were 49 +/- 4, 59 +/- 4, 16 +/- 4, and 33 +/- 4 mg x kg(-1) x min(-1) for CHD-WT, CHD-HET, HFD-WT, and HFD-HET mice, respectively, showing that HET limited the severity of whole-body insulin resistance with HFD. Insulin-stimulated muscle glucose utilization was attenuated in HFD-WT but unaffected in HFD-HET mice. Conversely, rates of LCFA clearance were increased with HFD feeding in HFD-WT but not in HFD-HET mice. In conclusion, a partial reduction in H-FABP protein normalizes fasting glucose levels and improves whole-body insulin sensitivity in HFD-fed mice despite obesity.
Considerations in the Design of Hyperinsulinemic-euglycemic Clamps in the Conscious Mouse Diabetes. Feb, 2006 | Pubmed ID: 16443772 Despite increased use of the hyperinsulinemic-euglycemic clamp to study insulin action in mice, the effects of experimental parameters on the results obtained have not been addressed. In our studies, we determined the influences of sampling sites, fasting duration, and insulin delivery on results obtained from clamps in conscious mice. Carotid artery and jugular vein catheters were implanted in C57BL/6J mice (n = 6-10/group) fed a normal diet for sampling and infusions. After a 5-day recovery period, mice underwent a 120-min clamp (2.5-mU . kg(-1) . min(-1) insulin infusion; approximately 120-130 mg/dl glucose) while receiving [3-(3)H]glucose to determine glucose appearance (endoR(a)) and disappearance (R(d)). Sampling large volumes (approximately 100 mul) from the cut tail resulted in elevated catecholamines and basal glucose compared with artery sampling. Catecholamines were not elevated when taking small samples ( approximately 5 mul) from the cut tail. Overnight (18-h) fasting resulted in greater loss of total body, lean, and fat masses and hepatic glycogen but resulted in enhanced insulin sensitivity compared with 5-h fasting. Compared with a 16-mU/kg insulin prime, a 300-mU/kg prime resulted in hepatic insulin resistance and slower acquisition of steady-state glucose infusion rates (GIR) after a 5-h fast. The steady-state GIR was expedited after the 300-mU/kg prime in 18-h-fasted mice. The GIR and R(d) rose with increasing insulin infusions (0.8, 2.5, 4, and 20 mU . kg(-1) . min(-1)), but endoR(a) was fully suppressed with doses higher than 0.8 mU . kg(-1) . min(-1). Thus, common variations in experimental factors yield different results and should be considered in designing and interpreting clamps.
Chronic Treatment with Sildenafil Improves Energy Balance and Insulin Action in High Fat-fed Conscious Mice Diabetes. Apr, 2007 | Pubmed ID: 17229936 Stimulation of nitric oxide-cGMP signaling results in vascular relaxation and increased muscle glucose uptake. We show that chronically inhibiting cGMP hydrolysis with the phosphodiesterase-5 inhibitor sildenafil improves energy balance and enhances in vivo insulin action in a mouse model of diet-induced insulin resistance. High-fat-fed mice treated with sildenafil plus L-arginine or sildenafil alone for 12 weeks had reduced weight and fat mass due to increased energy expenditure. However, uncoupling protein-1 levels were not increased in sildenafil-treated mice. Chronic treatment with sildenafil plus L-arginine or sildenafil alone increased arterial cGMP levels but did not adversely affect blood pressure or cardiac morphology. Sildenafil treatment, with or without l-arginine, resulted in lower fasting insulin and glucose levels and enhanced rates of glucose infusion, disappearance, and muscle glucose uptake during a hyperinsulinemic (4 mU x kg(-1) x min(-1))-euglycemic clamp in conscious mice. These effects occurred without an increase in activation of muscle insulin signaling. An acute treatment of high fat-fed mice with sildenafil plus l-arginine did not improve insulin action. These results show that phosphodiesterase-5 is a potential target for therapies aimed at preventing diet-induced energy imbalance and insulin resistance.
Glucose Kinetics and Exercise Tolerance in Mice Lacking the GLUT4 Glucose Transporter The Journal of Physiology. Jul, 2007 | Pubmed ID: 17495042 The absence of GLUT4 severely impairs basal glucose uptake in vivo, but does not alter glucose homeostasis or circulating insulin. Glucose uptake in isolated contracting skeletal muscle (MGU) is also impaired by the absence of GLUT4, and onset of muscle fatigue is hastened. Whether the body can compensate and preserve glucose homeostasis during exercise, as it does in the basal state, is unknown. One aim was to test the effectiveness of glucoregulatory compensation for the absence of GLUT4 in vivo. The absence of GLUT4 was also used to further define the role of hexokinase (HK) II, which catalyses glucose phosphorylation after it is transported in the cell. HK II increases MGU during exercise, as well as exercise endurance. In the absence of GLUT4, HK II expression will not affect MGU. A second aim was to test whether, in the absence of GLUT4, HK II retains its ability to increase exercise endurance. Wild-type (WT), GLUT4 null (GLUT4(-/-)), and GLUT4 null overexpressing HK II (GLUT4(-/-)HK(Tg)) mice were studied using a catheterized mouse model that allows blood sampling and isotope infusions during treadmill exercise. The impaired capacity of working muscle to take up glucose in GLUT4(-/-) is partially offset by an exaggerated increase in the glucagon: insulin ratio, increased liver glucose production, hyperglycaemia, and a greater capillary density in order to increase the delivery of glucose to the exercising muscle of GLUT4(-/-). Hearts of GLUT4(-/-) also exhibited a compensatory increase in HK II expression and a paradoxical increase in glucose uptake. Exercise tolerance was reduced in GLUT4(-/-) compared to WT. As expected, MGU in GLUT4(-/-)HK(Tg) was the same as in GLUT4(-/-). However, HK II overexpression retained its ability to increase exercise endurance. In conclusion, unlike the basal state where glucose homeostasis is preserved, hyperglycaemia results during exercise in GLUT4(-/-) due to a robust stimulation of liver glucose release in the face of severe impairments in MGU. Finally, studies in GLUT4(-/-)HK(Tg) show that HK II improves exercise tolerance, independent of its effects on MGU.
Phosphorylation Barriers to Skeletal and Cardiac Muscle Glucose Uptakes in High-fat Fed Mice: Studies in Mice with a 50% Reduction of Hexokinase II Diabetes. Oct, 2007 | Pubmed ID: 17639019 Muscle glucose uptake (MGU) is regulated by glucose delivery to, transport into, and phosphorylation within muscle. The aim of this study was to determine the role of limitations in glucose phosphorylation in the control of MGU during either physiological insulin stimulation (4 mU x kg(-1) x min(-1)) or exercise with chow or high-fat feeding.
Insulin Action in the Double Incretin Receptor Knockout Mouse Diabetes. Feb, 2008 | Pubmed ID: 17977951 The incretins glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide have been postulated to play a role in regulating insulin action, although the mechanisms behind this relationship remain obscure. We used the hyperinsulinemic-euglycemic clamp to determine sites where insulin action may be modulated in double incretin receptor knockout (DIRKO) mice, which lack endogenous incretin action.
Metabolic Implications of Reduced Heart-type Fatty Acid Binding Protein in Insulin Resistant Cardiac Muscle Biochimica Et Biophysica Acta. Oct, 2008 | Pubmed ID: 18692568 Insulin resistance is characterized by elevated rates of cardiac fatty acid utilization resulting in reduced efficiency and cardiomyopathy. One potential therapeutic approach is to limit the uptake and oxidation of fatty acids. The aims of this study were to determine whether a quantitative reduction in heart-type fatty acid binding protein (FABP3) normalizes cardiac substrate utilization without altering cardiac function. Transgenic (FABP3(+/-)) and wild-type (WT) littermates were studied following low fat (LF) or high fat (HF) diets, with HF resulting in obese, insulin-resistant mice. Cardiovascular function (systolic blood pressure, % fractional shortening) and heart dimension were measured at weaning and every month afterward for 3 mo. During this period cardiovascular function was the same independent of genotype and diet. Catheters were surgically implanted in the carotid artery and jugular vein for sampling and infusions in mice at 4 mo of age. Following 5 d recovery, mice underwent either a saline infusion or a hyperinsulinemic-euglycemic clamp (4 mU kg(-1) min(-1)). Indices of long chain fatty acid and glucose utilization (R(f), R(g); mumol g wet weight(-1) min(-1)) were obtained using 2-deoxy[(3)H]glucose and [(125)I]-15-rho-iodophenyl)-3-R,S-methylpentadecanoic acid. FABP3(+/-) had enhanced cardiac R(g) compared with WT during saline infusion in both LF and HF. FABP3(+/-) abrogated the HF-induced decrement in insulin-stimulated cardiac R(g). On a HF diet, FABP(+/-) but not WT had an increased reliance on fatty acids (R(f)) during insulin stimulation. In conclusion, cardiac insulin resistance and glucose uptake is largely corrected by a reduction in FABP3 in vivo without contemporaneous deleterious effects on cardiac function.
The Glucagon-like Peptide-1 Receptor Regulates Endogenous Glucose Production and Muscle Glucose Uptake Independent of Its Incretin Action Endocrinology. Mar, 2009 | Pubmed ID: 19008308 Glucagon-like peptide-1 (GLP-1) diminishes postmeal glucose excursions by enhancing insulin secretion via activation of the beta-cell GLP-1 receptor (Glp1r). GLP-1 may also control glucose levels through mechanisms that are independent of this incretin effect. The hyperinsulinemic-euglycemic clamp (insulin clamp) and exercise were used to examine the incretin-independent glucoregulatory properties of the Glp1r because both perturbations stimulate glucose flux independent of insulin secretion. Chow-fed mice with a functional disruption of the Glp1r (Glp1r(-/-)) were compared with wild-type littermates (Glp1r(+/+)). Studies were performed on 5-h-fasted mice implanted with arterial and venous catheters for sampling and infusions, respectively. During insulin clamps, [3-(3)H]glucose and 2[(14)C]deoxyglucose were used to determine whole-body glucose turnover and glucose metabolic index (R(g)), an indicator of glucose uptake. R(g) in sedentary and treadmill exercised mice was determined using 2[(3)H]deoxyglucose. Glp1r(-/-) mice exhibited increased glucose disappearance, muscle R(g), and muscle glycogen levels during insulin clamps. This was not associated with enhanced muscle insulin signaling. Glp1r(-/-) mice exhibited impaired suppression of endogenous glucose production and hepatic glycogen accumulation during insulin clamps. This was associated with impaired liver insulin signaling. Glp1r(-/-) mice became significantly hyperglycemic during exercise. Muscle R(g) was normal in exercised Glp1r(-/-) mice, suggesting that hyperglycemia resulted from an added drive to stimulate glucose production. Muscle AMP-activated protein kinase phosphorylation was higher in exercised Glp1r(-/-) mice. This was associated with increased relative exercise intensity and decreased exercise endurance. In conclusion, these results show that the endogenous Glp1r regulates hepatic and muscle glucose flux independent of its ability to enhance insulin secretion.
Skeletal Muscle AMP-activated Protein Kinase is Essential for the Metabolic Response to Exercise in Vivo The Journal of Biological Chemistry. Sep, 2009 | Pubmed ID: 19525228 AMP-activated protein kinase (AMPK) has been postulated as a super-metabolic regulator, thought to exert numerous effects on skeletal muscle function, metabolism, and enzymatic signaling. Despite these assertions, little is known regarding the direct role(s) of AMPK in vivo, and results obtained in vitro or in situ are conflicting. Using a chronically catheterized mouse model (carotid artery and jugular vein), we show that AMPK regulates skeletal muscle metabolism in vivo at several levels, with the result that a deficit in AMPK activity markedly impairs exercise tolerance. Compared with wild-type littermates at the same relative exercise capacity, vascular glucose delivery and skeletal muscle glucose uptake were impaired; skeletal muscle ATP degradation was accelerated, and arterial lactate concentrations were increased in mice expressing a kinase-dead AMPKalpha2 subunit (alpha2-KD) in skeletal muscle. Nitric-oxide synthase (NOS) activity was significantly impaired at rest and in response to exercise in alpha2-KD mice; expression of neuronal NOS (NOSmicro) was also reduced. Moreover, complex I and IV activities of the electron transport chain were impaired 32 +/- 8 and 50 +/- 7%, respectively, in skeletal muscle of alpha2-KD mice (p < 0.05 versus wild type), indicative of impaired mitochondrial function. Thus, AMPK regulates neuronal NOSmicro expression, NOS activity, and mitochondrial function in skeletal muscle. In addition, these results clarify the role of AMPK in the control of muscle glucose uptake during exercise. Collectively, these findings demonstrate that AMPK is central to substrate metabolism in vivo, which has important implications for exercise tolerance in health and certain disease states characterized by impaired AMPK activation in skeletal muscle.
Endothelial Nitric Oxide Synthase is Central to Skeletal Muscle Metabolic Regulation and Enzymatic Signaling During Exercise in Vivo American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. May, 2010 | Pubmed ID: 20200137 Endothelial nitric oxide synthase (eNOS) is associated with a number of physiological functions involved in the regulation of metabolism; however, the functional role of eNOS is poorly understood. We tested the hypothesis that eNOS is critical to muscle cell signaling and fuel usage during exercise in vivo, using 16-wk-old catheterized (carotid artery and jugular vein) C57BL/6J mice with wild-type (WT), partial (+/-), or no expression (-/-) of eNOS. Quantitative reductions in eNOS expression ( approximately 40%) elicited many of the phenotypic effects observed in enos(-/-) mice under fasted, sedentary conditions, with expression of oxidative phosphorylation complexes I to V and ATP levels being decreased, and total NOS activity and Ca(2+)/CaM kinase II Thr(286) phosphorylation being increased in skeletal muscle. Despite these alterations, exercise tolerance was markedly impaired in enos(-/-) mice during an acute 30-min bout of exercise. An eNOS-dependent effect was observed with regard to AMP-activated protein kinase signaling and muscle perfusion. Muscle glucose and long-chain fatty acid uptake, and hepatic and skeletal muscle glycogenolysis during the exercise bout was markedly accelerated in enos(-/-) mice compared with enos(+/-) and WT mice. Correspondingly, enos(-/-) mice exhibited hypoglycemia during exercise. Thus, the ablation of eNOS alters a number of physiological processes that result in impaired exercise capacity in vivo. The finding that a partial reduction in eNOS expression is sufficient to induce many of the changes associated with ablation of eNOS has implications for chronic metabolic diseases, such as obesity and insulin resistance, which are associated with reduced eNOS expression.
Glucagon-like Peptide-1 Receptor Knockout Mice Are Protected from High-fat Diet-induced Insulin Resistance Endocrinology. Oct, 2010 | Pubmed ID: 20685876 Glucagon-like peptide-1 augments nutrient-stimulated insulin secretion. Chow-fed mice lacking the glucagon-like peptide-1 receptor (Glp1r) exhibit enhanced insulin-stimulated muscle glucose uptake but impaired suppression of endogenous glucose appearance (endoRa). This proposes a novel role for the Glp1r to regulate the balance of glucose disposal in muscle and liver by modulating insulin action. Whether this is maintained in an insulin-resistant state is unknown. The present studies tested the hypothesis that disruption of Glp1r expression overcomes high-fat (HF) diet-induced muscle insulin resistance and exacerbates HF diet-induced hepatic insulin resistance. Mice with a functional disruption of the Glp1r (Glp1r-/-) were compared with wild-type littermates (Glp1r+/+) after 12 wk on a regular chow diet or a HF diet. Arterial and venous catheters were implanted for sampling and infusions. Hyperinsulinemic-euglycemic clamps were performed on weight-matched male mice. [3-(3)H]glucose was used to determine glucose turnover, and 2[14C]deoxyglucose was used to measure the glucose metabolic index, an indicator of glucose uptake. Glp1r-/- mice exhibited increased glucose disappearance and muscle glucose metabolic index on either diet. This was associated with enhanced activation of muscle Akt and AMP-activated protein kinase and reduced muscle triglycerides in HF-fed Glp1r-/- mice. Chow-fed Glp1r-/- mice exhibited impaired suppression of endoRa and hepatic insulin signaling. In contrast, HF-fed Glp1r-/- mice exhibited improved suppression of endoRa and hepatic Akt activation. This was associated with decreased hepatic triglycerides and impaired activation of sterol regulatory element-binding protein-1. These results show that mice lacking the Glp1r are protected from HF diet-induced muscle and hepatic insulin resistance independent of effects on total fat mass.


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Cool Steely Dan Back on step and trip As clocking says, Now would hardly appear to be the right moment for the first Steely Dan tour since 1974, Which stumbled on Madison Square Garden on sunday night.
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Quick Reference
(b Paris, probably 1676 or 1677; d Paris, 6 Aug. 1739)
French dancer, choreographer and teacher. He played an important role in the early development of dance in Paris. He was the nephew and pupil of Beauchamps and joined the Paris Opera in the 1690s, where he performed in ballets and operas by Lully and Campra. In 1729, already established as the leading danseur noble of his day, he became compositeur des ballets de l'Académie Royale de Musique (dance director of the Paris Opera). His best-known work was Les Amours des déesses (mus. Quinault, 1729). As a teacher, his students included Sallé and Camargo.
Subjects: Dance.
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Summer Reading
The objective of summer reading is to provide students with meaningful, relevant selections that will help foster their critical reading and analytical skills and hopefully spark a new curiosity and appreciation for literature, as well as the wondrous world around them.
We provide a variety of assessments, including projects, writing assignments, and objective tests. English teachers will provide specific instructions and dates within the first two weeks of school. The assessments enable our students to demonstrate their comprehension of the books they read, as well as their ability to analyze and connect with the literature.
Use the links below for grade level reading assignments or click HERE for a printable PDF.


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Calling 9-1-1: Fairfax Prepares Day 21
Posted 3:42 p.m.
It may seem obvious – call 9-1-1 for an emergency.
But in a high-stress situation, do you know what information is needed? Is your home clearly marked. Do you know the public safety non-emergency phone number?
Here are a few tips to consider when calling 9-1-1:
- Use 9-1-1 for emergencies only.
- Stay calm and help the call taker help you.
- Determine the location of the emergency, if possible, before you call.
- Texting 9-1-1 is NOT an option; you must dial 9-1-1 and speak with a call taker.
- Teach your children how to call 9-1-1.
- Do not give old phones to children as toys. A wireless phone with no active service can still dial 9-1-1.
- If you accidentally call 9-1-1, stay on the line and tell the call taker that you do not have an emergency.
- Post your home address clearly and prominently so first responders can find you.
- Pull over when driving, if possible. This reduces the chance of a dropped call.
- Tips for non-English callers and hearing or speech-impaired callers.
We receive more than 1 million 9-1-1 calls a year. Hopefully you don't have to call, but if you do, make sure it's an emergency. If you're not sure, call 9-1-1, but if it's clearly a non-emergency, then call the non-emergency number.
THE ASK: 9-1-1 is an easy to remember phone number, but you can help reduce unnecessary calls if your situation is not an emergency. This weekend, add a new contact to your phones for the public safety non-emergency number at 703-691-2131, TTY 711.
TELL US you've done this:
- Post a quick reply in this blog's comments section below such as "I've done this."
- Use the Twitter hashtag #fairfaxprepares and tweet your accomplishment. Include photos if you'd like.
- Like our special Facebook page for this campaign to leave comments and share tips with your friends.
- Email us at firstname.lastname@example.com that you accomplished an ask.
- Click the links below to email, share on social media or print a hard copy. Thanks!
9 responses to "Calling 9-1-1: Fairfax Prepares Day 21"
Flora/Jerri Lyn (@florajl) says :
Just updated my Blackberry!
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- September 30, 2012 -


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Main → Afghanistan → Velayat Ghowr → Taygh-e Khanim
Map of Taygh-e Khanim Velayat Ghowr, Afghanistan
Other Names: Gora Khanim,Taygh-e Khanim,Taygh-e Khāṉim,Teghe Khanem,Teghe Khāṉem,Tigh-e Khanom,Tīgh-e Khānom,تیغ خاڼم, Taygh-e Khāṉim
Taygh-e Khanim
Welcome to the Taygh-e Khanim google satellite map! This mountain is situated in Velayat Ghowr, Afghanistan. Original name (with diacritics) of the place is Taygh-e Khāṉim. See Taygh-e Khanim photos and images from satellite below, explore the aerial photographs of Taygh-e Khāṉim area. This placemark was added 2005-10-28.
Map of Taygh-e Khanim
- Country: Afghanistan
- Province: Velayat Ghowr
- Category: mountain
- Altitude: 0 m
- Population: 0
Asia/Kabul +4.5
- Local Time: 07:18
- Sunrise: 05:38
- Sunset: 18:55
Wiki articles near Taygh-e Khanim
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- Services
- We strive to provide complete care for our patients. Learn more about all the services we provide.
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Basketball Diaries {& Giveaway}
This past weekend Jason and I took the kids to see the Harlem Globetrotters at the Barclay Center in Brooklyn! I love anything that takes place at the Barclay's because it becomes a fun escape to Brooklyn for us, and the fairly new arena is always such a treat! The…Read More


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Celebrity fight fans have lashed out at boxing officials following the controversial split decision which ended Manny Pacquiao's winning streak on Saturday night (09Jun12) in Las Vegas, insisting the big event was clearly "rigged".
Josh Duhamel, Miley Cyrus and Ashlee Simpson were among those who took to Twitter.com after Timothy Bradley was declared the winner - even though Pacquaio landed more punches than the contender in 10 of the 12 rounds and, in most people's eyes, was the clear winner of the welterweight fight - to vent their disgust.
Simpson wrote, "#shameonboxing. I think I will stick to... (reality TV show) so you think you can dance."
And fight fan Cyrus added, "This just proves that everything boils down to politics. ugh. why cant people just fight fair?! let the WINNERS win!"
Transformers star Duhamel was just as disgusted, tweeting, "Yet ANOTHER reason why boxing sucks. #RIGGED."


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Having Trouble Scheduling Events - It keeps telling me they are conflicting
Discussions about the Calendar Tool at lds.org. Questions about the calendar on the classic site should be posted in the LUWS forum.
5 posts • Page 1 of 1
Having Trouble Scheduling Events - It keeps telling me they are conflicting
For some reason when I try to schedule the building, and I've designated different rooms for each event, it won't let me schedule more than one event on any given day. It keeps telling me the events are conflicting even though they are using separate rooms. Any ideas?
- Community Administrator
- Posts: 24191
- Joined: Sat Jan 20, 2007 2:53 pm
- Location: U.S.
Do you have a event that's using the "whole facility"?
Is this a conflict that prevents you from saving, or just an advisory?
Is this a conflict that prevents you from saving, or just an advisory?
Have you searched the Wiki?
Try using a Google search by adding "site:tech.lds.org/wiki" to the search criteria.
Try using a Google search by adding "site:tech.lds.org/wiki" to the search criteria.
ASpaugh wrote:No, each event is using only one room, and it will not let me save it.
If it won't let you save, then the conflicting event will be shown to you in the popup where you are entering the event details. You need to take note of the conflicting event(s) and edit that event to see its details. It seems likely that you will find that it is using the whole location during a conflicting time.
It's also possible that the building has been assigned to a different unit during the time you are trying to schedule. If that's the case, you need to contact the building scheduler to work this out. The scheduler's contact info should also be listed by the event on that popup.
Questions that can benefit the larger community should be asked in a public forum, not a private message.
I'm the Stake Administrator and I schedule the buildings as well. I looked into every possible problem, but none could be found. Each event was in a separate room in the Stake Center, so there shouldn't have been a conflict even though they were there at the same time. In one instance I was able to delete all the events for that particular day, and then put them back on one by one in reverse order and it worked that way. So not a true solution, I just worked around it.
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To the Editor:
"There you go again" is the phrase that Ronald Reagan used during many of his campaign speeches to shut down his parroting opponent.
I am sick and tired of the "Lefties" vilifying the "Rich." Who are the "Rich"? They are the taxpayers who provide us all with benefits through government theft. They are also another target of the left, through the use of group identity politics, to create victims (themselves) that big government needs to save.
In this world there will always be people among us who are smarter, more talented and more ambitious than the rest of us. They, through their own actions, become rich. They work harder and are more successful than us. They do not make us victims. We make ourselves victims by our own mediocrity.
Like it or not we live in a meritocracy where hard work and brains are rewarded. By our own founding documents we are blessed with equality of Opportunity, not equality of outcome.
Richard T. Todd


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These painted hangers are a nice & special touch for hanging your wedding gown and bridesmaid's dresses on. They can cost quite a lot each to have painted for you.
Don't think you can wield a paintbrush steadily enough to pull this off? No problem!! Craft stores carry decals that can be rubbed directly onto the hanger with a popsicle stick.
Paint pens have made me look like an actual artist in the past!! This marvelous invention is a pen that writes with paint instead of ink. Perfect for handwriting names or sentimental sayings onto projects.
When you are done, paint on a layer of Mod Podge to seal it all in.
Click here for a good tutorial on painting and heat-setting your glasses. I used this as a guideline to make some glass coffee mugs for Christmas gifts, and they have held up nicely.
|A few sample ideas for some patterns that you can try.
Next is the very best tip I have ever come across for making this craft work. (Yes, once again, thank you Pinterest!!)
Print out or draw your design on a piece of paper, tape it INSIDE the glass, then trace.
Oh yeah!! Way easier than trying it freehand.
Go ahead, set aside an evening or afternoon and give one of these a try. You can do it!!


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Almost Done
This move is going to go down in history as the longest ever.
We go back to Houghton tonight to meet the movers tomorrow and get our stuff delivered on Thursday.
Really, it hasn't been that long. It's just that patience is a virtue I'm lacking.
Big time.
Also, why am I having such a hard time getting used to central time?
I need a good night of sleep.
Or a venti caramel machiatto.
Whatever works :)


text: Q-As you know, it is hard to get people to serve on a condo board of directors. A woman on our board is licensed as a decorator in the state and serves on the decorating as well as the membership committee. In her capacity, this board member has been given the power and authority to approve all purchasing. That is, everything that is bought for the condo must first be approved by her. In addition, she signs the checks. It seems to some of us that she has too much individual power and probably profits from her decorating purchases. But since it is difficult to find working board members, the president is happy to have her. Is there anything that can be done?