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blood. When blood glucose levels rise (after a meal, for example), insulin is secreted from the pancreas into the pancreatic vein, which empties into the portal vein system (Figure 23.21), so that insulin traverses the liver before it enters the systemic blood supply. Insulin acts to rapidly lower blood glucose concentration in several ways. Insulin stimulates glycogen synthesis and inhibits glycogen breakdown in liver and muscle.

Several other physiological effects of insulin also serve to lower blood and tissue glucose levels (Figure 23.22). Insulin stimulates the active transport of glucose (and amino acids) across the plasma membranes of muscle and adipose tissue. Insulin also increases cellular utilization of glucose by inducing the synthesis of several important glycolytic enzymes, namely, glucokinase, phos-phofructokinase, and pyruvate kinase. In addition, insulin acts to inhibit several enzymes of gluconeogenesis. These various actions enable the organism to respond quickly to increases in blood glucose levels.

Glucagon and Epinephrine Stimulate Glycogen Breakdown

Catabolism of tissue glycogen is triggered by the actions of the hormones epi-nephrine and glucagon (Figure 23.23). In response to decreased blood glucose, glucagon is released from the a cells in pancreatic islets of Langerhans. This peptide hormone travels through the blood to specific receptors on liver cell membranes. (Glucagon is active in liver and adipose tissue, but not in other tissues.) Similarly, signals from the central nervous system cause release of epinephrine (Figure 23.24)—also known as adrenaline—from the adrenal glands into the bloodstream. Epinephrine acts on liver and muscles. When either hormone binds to its receptor on the outside surface of the cell membrane, a cascade is initiated that activates glycogen phosphorylase and inhibits glycogen synthase. The result of these actions is tightly coordinated stimulation of glycogen breakdown and inhibition of glycogen synthesis.

Active transport +

Glycolysis

Glycogen synthesis

Insulin

Insulin receptor

Protein phosphorylation and second messenger modulation

Insulin receptor

Lipid synthesis

Gluconeogenesis

+ Protein synthesis

Lipid breakdown

FIGURE 23.22 • The metabolic effects of insulin. As described in Chapter 34, binding of insulin to membrane receptors stimulates the protein kinase activity of the receptor. Subsequent phosphorylation of target proteins modulates the effects indicated.

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