Insulin and glucagon, along with the catecholamines, such as epinephrine, play a crucial role in regulating energy metabolism (Fig. 23.16). Insulin, a peptide hormone produced by the β cells of the pancreas, primarily controls the integration of energy metabolism. It consists of disulfide-linked A and B chains. When blood glucose levels rise, insulin secretion is stimulated. Insulin acts as an anabolic hormone by increasing glucose uptake through glucose transporters (GLUT-4) in muscle and adipose tissue. It also enhances the synthesis of glycogen, protein, and triacylglycerol. These effects are mediated by binding to its membrane tyrosine kinase receptor and initiating a series of cell-signaling responses. Glucagon, on the other hand, is a monomeric peptide hormone produced by the α cells of the pancreatic islets. It acts as a catabolic hormone and opposes many of the actions of insulin. Glucagon helps maintain blood glucose levels during potential hypoglycemia. It increases glycogenolysis, gluconeogenesis, fatty acid oxidation, ketogenesis, and amino acid uptake. Glucagon secretion is stimulated by low blood glucose, amino acids, and the catecholamines. Its secretion is inhibited by elevated blood glucose and insulin. Glucagon binds to high-affinity G protein–coupled receptors on hepatocyte cell membranes, leading to the activation of adenylyl cyclase and subsequent production of cyclic adenosine monophosphate (cAMP) as a second messenger. Activation of cAMP-dependent protein kinase A then phosphorylates key regulatory enzymes involved in carbohydrate and lipid metabolism. Insulin and glucagon both have an impact on gene transcription.
Hypoglycemia, characterized by low blood glucose levels, is accompanied by adrenergic and neuroglycopenic symptoms that can be rapidly resolved by administering glucose. Glucagon and epinephrine are released in response to insulin-induced, postprandial, and fasting hypoglycemia. Ethanol metabolism causes an increase in nicotinamide adenine dinucleotide (NADH), which inhibits gluconeogenesis, leading to hypoglycemia in individuals with depleted stores. Alcohol consumption also raises the risk of hypoglycemia in patients using insulin. Furthermore, chronic alcohol consumption can result in fatty liver disease.
Now, let's address the question:
3.1. Which of the following statements is true for insulin but not for glucagon?
A. It is a peptide hormone secreted by pancreatic cells.
B. Its actions are mediated by binding to a receptor found on the cell membrane of liver cells.
C. Its effects include alterations in gene expression.
D. Its secretion is decreased by the catecholamines.
E. Its secretion is increased by amino acids.
F. Its synthesis involves a nonfunctional precursor that gets cleaved to yield a functional molecule.

Answer: C. Its effects include alterations in gene expression.
The integration of energy metabolism is controlled primarily by insulin and the opposing actions of glucagon and the catecholamines, particularly epinephrine (Fig. 23.16). Changes in the circulating levels of these hormones allow the body to store energy when food is abundant or to make stored energy available in times of physiologic stress (for example, during survival crises, such as famine). Insulin is a peptide hormone produced by the β cells of the islets of Langerhans of the pancreas. It consists of disulfide-linked A and B chains. A rise in blood glucose is the most important signal for insulin secretion. The catecholamines, secreted in response to stress, trauma, or extreme exercise, inhibit insulin secretion. Insulin increases glucose uptake (by glucose transporters (GLUT-4) in muscle and adipose tissue) and the synthesis of glycogen, protein, and triacylglycerol: It is an anabolic hormone. These actions are mediated by binding to its membrane tyrosine kinase receptor. Binding initiates a cascade of cell-signaling responses, including phosphorylation of a family of proteins called insulin receptor substrate proteins. Glucagon is a monomeric peptide hormone produced by the α cells of the pancreatic islets (both insulin and glucagon synthesis involve formation of inactive precursors that are cleaved to form the active hormones). Glucagon, along with epinephrine, norepinephrine, cortisol, and growth hormone (the counterregulatory hormones), opposes many of the actions of insulin. Glucagon acts to maintain blood glucose during periods of potential hypoglycemia. Glucagon increases glycogenolysis, gluconeogenesis, fatty acid oxidation, ketogenesis, and amino acid uptake: It is a catabolic hormone. Glucagon secretion is stimulated by low blood glucose, amino acids, and the catecholamines. Its secretion is inhibited by elevated blood glucose and by insulin. Glucagon binds to high-affinity G protein–coupled receptors on the cell membrane of hepatocytes. Binding results in the activation of adenylyl cyclase, which produces the second messenger cyclic adenosine monophosphate (cAMP). Subsequent activation of cAMPdependent protein kinase A results in the phosphorylation-mediated activation or inhibition of key regulatory enzymes involved in carbohydrate and lipid metabolism. Both insulin and glucagon affect gene transcription.
Hypoglycemia is characterized by low blood glucose accompanied by adrenergic and neuroglycopenic symptoms that are rapidly resolved by the administration of glucose. Insulin-induced, postprandial, and fasting hypoglycemia result in release of glucagon and epinephrine. The rise in nicotinamide adenine dinucleotide (NADH) that accompanies ethanol metabolism inhibits gluconeogenesis, leading to hypoglycemia in individuals with depleted stores. Alcohol consumption also increases the risk for hypoglycemia in patients using insulin. Chronic alcohol consumption can cause fatty liver disease.
Choose the ONE best answer.
3.1. Which of the following statements is true for insulin but not for glucagon?
A. It is a peptide hormone secreted by pancreatic cells.
B. Its actions are mediated by binding to a receptor found on the cell membrane of liver cells.
C. Its effects include alterations in gene expression.
D. Its secretion is decreased by the catecholamines.
E. Its secretion is increased by amino acids.
F. Its synthesis involves a nonfunctional precursor that gets cleaved to yield a functional molecule.