Hypoglycemia attenuates acute amylin-induced reduction of food intake in male rats

The ability of amylin to inhibit gastric emptying and glucagon secretion in rats is reduced under hypoglycemic conditions. These effects are considered part a fail-safe mechanism that prevents from further decreasing nutrient supply when blood glucose levels low. Because these actions amylin-induced satiation mediated by the area postrema (AP), it plausible phenomena based on co-sensitivity AP neurons glucose. Using hyperinsulinemic clamps unrestrained freely-feeding rats, we investigated whether amylin's food intake also hypoglycemia (HYPO). Following an 18 h fast, were infused with insulin for 45 min clamp at baseline (between 90 100 mg/dL). HYPO (approximately 55 mg/dL) was induced between 60 then maintained remainder clamp. Rats injected (20 µg/kg) or saline offered normal chow 85 min. Food measured 30 after amylin. Control hyperinsulinemic/euglycemic (EU) approximately 150 mg/dL (which physiological periprandial level) before injection. Terminal experiments tested effect induce phosphorylation ERK, marker action AP, EU Amylin significantly 30- 60-min but attenuated rats. Interestingly, infusion rate had be dramatically meal onset saline-treated, not amylin-treated, rats; this suggests meal-related appearance inhibited both HYPO. Finally, similar pERK response We conclude decrease eating blunted hypoglycemia, seems downstream neurons. data allow us extend idea brake its intake-reducing effect, demonstrate can buffer meal-induced levels.