Instruct: Given a question, retrieve passages that can help answer the question.
Query: What is reactive hypoglycemia?
Reactive hypoglycemia, postprandial hypoglycemia, or sugar crash is a term describing recurrent episodes of symptomatic hypoglycemia occurring within four hours after a high carbohydrate meal in people both with and without diabetes. The term is not necessarily a diagnosis since it requires an evaluation to determine the cause of the hypoglycemia.
Hypoglycemic symptoms can also occur when one is sleeping. Examples of symptoms during sleep can include damp bed sheets or clothes from perspiration. Having nightmares or the act of crying out can be a sign of hypoglycemia. Once the individual is awake they may feel tired, irritable, or confused and these may be signs of hypoglycemia as well.
Hypoglycemia, or low blood glucose, causes cardiovascular physiological effects as a result of the sympathoadrenal system. These physiological changes include an increased heart rate, increased heart contractility, and decreased peripheral arterial resistance. Together, the effects increase peripheral blood pressure, but decrease central blood pressure. This can have larger effects on those with diabetes. Hypoglycemia may cause greater arterial wall stiffness and less elasticity, which in turn decreases blood pressure and increases the heart’s workload. Symptoms of hypoglycemia related to the symapthoadrenal system include anxiety, tremors, irregular heartbeat, sweating, hunger, and paresthesia. Hypothermia and neurological deficits can also occur. Permanent brain damage is uncommon but have been seen in some who suffer from hypoglycemia. The activation of the system is assisted by norepinephrine, acetylcholine, and epinephrine. Hypoglycemia unawareness can occur because the symapthoadrenal system response is reduced, in turn, the symptoms are reduced. Since the symptoms go unnoticed, this may lead to a dangerous cycle of hypoglycemia and an increased risk of severe hypoglycemia, which can have serious consequences.
The signs of diabetes mellitus are caused by a persistently high blood glucose concentration, which may be caused by either insufficient insulin, or by a lack of response to insulin. Most cats have a type of diabetes mellitus similar to human diabetes mellitus type 2, with β-cell dysfunction and insulin resistance. Factors which contribute to insulin resistance include obesity and endocrine diseases such as acromegaly. Acromegaly affects 20–30% of diabetic cats; it can be diagnosed by measuring the concentration of insulin-like growth factor-1 (IGF-1) in the blood.
Signs and symptoms include: hypoglycemia, dehydration, weight loss, and disorientation. Additional signs and symptoms include weakness, tiredness, dizziness, low blood pressure that falls further when standing (orthostatic hypotension), cardiovascular collapse, muscle aches, nausea, vomiting, and diarrhea. These problems may develop gradually and insidiously. Addison's disease can present with tanning of the skin that may be patchy or even all over the body. Characteristic sites of tanning are skin creases (e.g. of the hands) and the inside of the cheek (buccal mucosa). Goitre and vitiligo may also be present. Eosinophilia may also occur.
Diabetes is a chronic metabolic disease characterized by increase blood glucose level. Type 2 diabetes is the most common form of diabetes. It is caused by resistance to insulin or the lack of production of insulin. It is seen most commonly in adults. Type 1 diabetes or juvenile diabetes affects mostly children. This condition is due to little or lack of insulin production from the pancreas.
The concept that insulin resistance may be the underlying cause of diabetes mellitus type 2 was first advanced by Professor Wilhelm Falta and published in Vienna in 1931, and confirmed as contributory by Sir Harold Percival Himsworth of the University College Hospital Medical Centre in London in 1936, however, type 2 diabetes does not occur unless there is concurrent failure of compensatory insulin secretion.
Type 2 diabetes mellitus, also known as non insulin dependent diabetes and as chronic hyperglycemia, is caused primarily by genetics and the development of obesity. The beta cells can still secrete insulin but the body has developed a resistance and its response to insulin has declined. It is believed to be due to the decline of specific receptors on the surface of the liver, adipose, and muscle cells which lose their ability to respond to insulin that circulates in the blood. In an effort to secrete enough insulin to overcome the increasing insulin resistance, the beta cells increase their function, size and number. Increased insulin secretion leads to hyperinsulinemia, but blood glucose levels remain within their normal range due to the decreased efficacy of insulin signaling. However, the beta cells can become overworked and exhausted from being overstimulated, leading to a 50% reduction in function along with a 40% decrease in beta-cell volume. At this point, not enough insulin can be produced and secreted to keep blood glucose levels within their normal range, causing overt type 2 diabetes.
Organ rejection is the unfortunate circumstance of the host immune system recognizing the transplanted organ as foreign. This is the most notable complication facing transplant recipients. Through T-cell receptors, T-lymphocytes are able to distinguish between self and non-self by recognizing human leukocyte antigens (HLA) bound to the major histocompatibility complex (MHC) protein located on the surface of organ cells. Once identified as foreign, the immune system proceeds to destroy the transplanted tissue. The panel reactive antibody (PRA) test measures the proportion of the population to which a recipient will react via pre-existing antibodies to various HLA antigens; in other words, how likely a patient is to acutely reject their new transplant. Therefore, it is essential that HLA and PRA statuses are tested for and demonstrate low immunoreactivity of the patient to the graft. In some cases, a recipient may suffer from graft-versus-host disease, in which cells of the transplanted organ attack the recipient's cells.
Group D
An active metabolite is an active form of a drug after it has been processed by the body.
Type 1 and type 2 diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with type 1 associated with youth and type 2 with being overweight. The term "mellitus" or "from honey" was added by the Briton John Rolle in the late 1700s to separate the condition from diabetes insipidus, which is also associated with frequent urination. Effective treatment was not developed until the early part of the 20th century, when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922. This was followed by the development of the long-acting insulin NPH in the 1940s.
Type 1 and type 2 diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 AD with type 1 associated with youth and type 2 with being overweight. The term "mellitus" or "from honey" was added by the Briton John Rolle in the late 1700s to separate the condition from diabetes insipidus which is also associated with frequent urination. Effective treatment was not developed until the early part of the 20th century when the Canadians Frederick Banting and Charles Best discovered insulin in 1921 and 1922. This was followed by the development of the long acting NPH insulin in the 1940s.
Diabetes is a monthly peer-reviewed medical journal published since 1952 by the American Diabetes Association. It covers research about the physiology and pathophysiology of diabetes mellitus including any aspect of laboratory, animal or human research. Emphasis is on investigative reports focusing on areas such as the pathogenesis of diabetes and its complications, normal and pathologic pancreatic islet function and intermediary metabolism, pharmacological mechanisms of drug and hormone action, and biochemical and molecular aspects of normal and abnormal biological processes. Diabetes also publishes abstracts presented at the ADA's annual meeting, Scientific Sessions, in as a supplement.
Treatment for hyperphosphatemia consists of treating the underlying disease, dialysis where appropriate, or oral administration of calcium carbonate, but not without first checking the serum calcium levels (these two levels are related). Administration of corticosteroids in gradually reduced doses (e.g., prednisolone) for 7–10 days is recommended by some specialists in cases of severe hemorrhagic effects. Organ-specific care and treatment are essential in cases of kidney, liver, or heart involvement.
Neither a cure for SS nor a specific treatment is known to permanently restore gland secretion. Instead, treatment is generally symptomatic and supportive.
Obesity has been found to contribute to approximately 55% of cases of type 2 diabetes; chronic obesity leads to increased insulin resistance that can develop into type 2 diabetes, most likely because adipose tissue (especially that in the abdomen around internal organs) is a source of several chemical signals, hormones and cytokines, to other tissues. Inflammatory cytokines such as TNFα may activate the NF-κB pathway which has been linked to the development of insulin resistance. Gene expression promoted by a diet of fat and glucose, as well as high levels of inflammation related cytokines found in the obese, can result in cells that "produce fewer and smaller mitochondria than is normal," and are thus prone to insulin resistance. Fat tissue has also been shown to be involved in managing much of the body's response to insulin and control of uptake of sugar. It secretes RBP4 which increases insulin resistance by blocking the action of insulin in muscle and liver. Fat cells also secrete adiponectin which acts in an opposite way to RBP4 by improving the action of insulin, however, engorged fat cells secrete it in lower amount than normal fat cells. The obese therefore may have higher level of RBP4 but lower level of adiponectin, both of which increase the risk of developing diabetes.
GDF2 has a role in inducing and maintaining the ability of embryonic basal forebrain cholinergic neurons (BFCN) to respond to a neurotransmitter called acetylcholine; BFCN are important for the processes of learning, memory and attention. GDF2 is also important for the maturation of BFCN. Another role of GDF2 has been recently suggested. GDF2 is a potent inducer of hepcidin (a cationic peptide that has antimicrobial properties) in liver cells (hepatocytes) and can regulate iron metabolism. The physiological receptor of GDF2 is thought to be activin receptor-like kinase 1, ALK1 (also called ACVRL1), an endothelial-specific type I receptor of the TGF-beta receptor family. Endoglin, a type I membrane glycoprotein that forms the TGF-beta receptor complex, is a co-receptor of ALK1 for GDF2/BMP-9 binding. Mutations in ALK1 and endoglin cause hereditary hemorrhagic telangiectasia (HHT), a rare but life-threatening genetic disorder that leads to abnormal blood vessel formation in multiple tissues and organs of the body.
Organisms typically cannot metabolize all types of carbohydrate to yield energy. Glucose is a nearly universal and accessible source of energy. Many organisms also have the ability to metabolize other monosaccharides and disaccharides but glucose is often metabolized first. In "Escherichia coli", for example, the lac operon will express enzymes for the digestion of lactose when it is present, but if both lactose and glucose are present the "lac" operon is repressed, resulting in the glucose being used first (see: Diauxie). Polysaccharides are also common sources of energy. Many organisms can easily break down starches into glucose; most organisms, however, cannot metabolize cellulose or other polysaccharides like chitin and arabinoxylans. These carbohydrate types can be metabolized by some bacteria and protists. Ruminants and termites, for example, use microorganisms to process cellulose. Even though these complex carbohydrates are not very digestible, they represent an important dietary element for humans, called dietary fiber. Fiber enhances digestion, among other benefits.
In human blood, glutamine is the most abundant free amino acid.
Group C
The prevalence of this condition is difficult to ascertain because a number of stricter or looser definitions have been used. It is recommended that the term reactive hypoglycemia be reserved for the pattern of postprandial hypoglycemia which meets the Whipple criteria (symptoms correspond to measurably low glucose and are relieved by raising the glucose), and that the term idiopathic postprandial syndrome be used for similar patterns of symptoms where abnormally low glucose levels at the time of symptoms cannot be documented.
According to the U.S. National Institutes of Health (NIH), a blood glucose level below 70 mg/dL (3.9 mmol/L) at the time of symptoms followed by relief after eating confirms a diagnosis for reactive hypoglycemia.
The NIH states: "The causes of most cases of reactive hypoglycemia are still open to debate. Some researchers suggest that certain people may be more sensitive to the body’s normal release of the hormone epinephrine, which causes many of the symptoms of hypoglycemia. Others believe deficiencies in glucagon secretion might lead to reactive hypoglycemia.
Stomach bypass surgery or hereditary fructose intolerance are believed to be causes, albeit uncommon, of reactive hypoglycemia. Myo-inositol or 1-"chiro"-inositol withdrawal can cause temporary reactive hypoglycemia.