Insulin Acts in the Arcuate Nucleus to Regulate Eating and Energy Conservation

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Insulin secretion reflects both the size of fat reserves (adiposity) and the current energy balance (blood glucose level). Insulin acts on insulin receptors in the hypothalamus to inhibit eating (Fig. 23-33). Insulin receptors in the orexigenic neurons of the arcuate nucleus inhibit the release of NPY, and insulin receptors in the anorexigenic neurons stimulate a-MSH production, thereby decreasing fuel intake and increasing thermo-genesis. By mechanisms discussed in Section 23.3, insulin also signals muscle, liver, and adipose tissues to increase catabolic reactions, including fat oxidation, which results in weight loss.

Leptin makes the cells of liver and muscle more sensitive to insulin. One hypothesis to explain this effect suggests cross-talk between the protein tyrosine kinases activated by leptin and those activated by insulin (Fig. 23-35); common second messengers in the two signaling pathways allow leptin to trigger some of the same downstream events that are triggered by insulin, through insulin receptor substrate-2 (IRS-2) and phos-phoinositide 3-kinase (PI-3K) (Chapter 12).

Insulin receptor

Insulin receptor

Insulin Receptors Nucelus

Inhibition of food intake

Inhibition of food intake

FIGURE 23-35 A possible mechanism for cross-talk between receptors for insulin and leptin. The insulin receptor has intrinsic Tyr kinase activity (see Fig. 12-6), and the leptin receptor, when occupied by its ligand, is phosphorylated by a soluble Tyr kinase (JAK). One possible explanation for the observed interaction between leptin and insulin is that both may phosphorylate the same substrate—in the case shown here, insulin receptor substrate-2 (IRS-2). When phosphorylated, IRS-2 activates PI-3K, which has downstream consequences that include inhibition of food intake. IRS-2 serves here as an integrator of the input from two receptors.

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