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首页> 外文期刊>Cell metabolism >Adiponectin stimulates AMP-activated protein kinase in the hypothalamus and increases food intake.
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Adiponectin stimulates AMP-activated protein kinase in the hypothalamus and increases food intake.

机译：脂联素刺激下丘脑中AMP激活的蛋白激酶并增加食物摄入量。

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摘要

Adiponectin has been shown to stimulate fatty acid oxidation and enhance insulin sensitivity through the activation of AMP-activated protein kinase (AMPK) in the peripheral tissues. The effects of adiponectin in the central nervous system, however, are still poorly understood. Here, we show that adiponectin enhances AMPK activity in the arcuate hypothalamus (ARH) via its receptor AdipoR1 to stimulate food intake; this stimulation of food intake by adiponectin was attenuated by dominant-negative AMPK expression in the ARH. Moreover, adiponectin also decreased energy expenditure. Adiponectin-deficient mice showed decreased AMPK phosphorylation in the ARH, decreased food intake, and increased energy expenditure, exhibiting resistance to high-fat-diet-induced obesity. Serum and cerebrospinal fluid levels of adiponectin and expression of AdipoR1 in the ARH were increased during fasting and decreased after refeeding. We conclude that adiponectin stimulates food intake and decreases energy expenditure during fasting through its effects in the central nervous system.
机译：脂联素已显示可通过激活外周组织中的AMP活化蛋白激酶（AMPK）来刺激脂肪酸氧化并增强胰岛素敏感性。然而，脂联素在中枢神经系统中的作用仍知之甚少。在这里，我们显示脂联素通过其受体AdipoR1刺激食物摄取增强弓形下丘脑（ARH）中的AMPK活性。脂联素对这种食物摄取的刺激被ARH中显性阴性AMPK表达减弱。此外，脂联素还减少了能量消耗。缺乏脂联素的小鼠在ARH中显示出AMPK磷酸化减少，食物摄入减少和能量消耗增加，表现出对高脂饮食诱导的肥胖的抵抗力。禁食期间血清和脑脊髓液中脂联素的水平以及AdipoR1的表达在禁食期间增加，而在再次喂养后降低。我们得出结论，脂联素通过禁食在中枢神经系统中的作用，可以刺激食物摄取并减少能量消耗。

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