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首页> 美国卫生研究院文献>other >CONTROL OF BLOOD PRESSURE APPETITE AND GLUCOSE BY LEPTIN IN MICE LACKING LEPTIN RECEPTORS IN POMC NEURONS
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CONTROL OF BLOOD PRESSURE APPETITE AND GLUCOSE BY LEPTIN IN MICE LACKING LEPTIN RECEPTORS IN POMC NEURONS

机译：瘦蛋白在缺乏POMC神经元瘦蛋白受体的小鼠中血压食欲和葡萄糖的控制

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Although the CNS melanocortin system is an important regulator of energy balance, the role of proopiomelanocortin (POMC) neurons in mediating the chronic effects of leptin on appetite, blood pressure, and glucose regulation is unknown. Using Cre/loxP technology we tested whether leptin receptor deletion in POMC neurons (LepRflox/flox/POMC-Cre mice) attenuates the chronic effects of leptin to increase mean arterial pressure (MAP), enhance glucose utilization and oxygen consumption (VO2), and reduce appetite. LepRflox/flox/POMC-Cre, wild-type (WT), LepRflox/flox and POMC-Cre mice were instrumented for MAP and heart rate (HR) measurement by telemetry, and venous catheters for infusions. LepRflox/flox/POMC-Cre mice were heavier, hyperglycemic, hyperinsulinemic, and hyperleptinemic compared to WT, LepRflox/flox and POMC-Cre mice. Despite exhibiting features of metabolic syndrome, LepRflox/flox/POMC-Cre mice had normal MAP and HR compared to LepRflox/flox but lower MAP and HR compared to WT mice. After a 5-day control period, leptin was infused (2 μg/kg/min, i.v.) for 7 days. In control mice, leptin increased MAP by ~5 mmHg despite decreasing food intake by ~35%. In contrast, leptin infusion in LepRflox/flox/POMC-Cre mice reduced MAP by ~3 mmHg and food intake by ~28%. Leptin significantly decreased insulin and glucose levels in control mice but not in LepRflox/flox/POMC-Cre mice. Leptin increased VO2 in LepRflox/flox/POMC-Cre and WT mice. Activation of POMC neurons is necessary for the chronic effects of leptin to raise MAP and reduce insulin and glucose levels, whereas leptin receptors in other areas of the brain besides POMC neurons appear to play a key role in mediating leptin’s chronic effects on appetite and VO2.

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