Overfeeding rapidly induces leptin and insulin resistance
Overfeeding rapidly induces leptin and insulin resistance
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DOI：
10.2337/diabetes.50.12.2786
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发表时间：
2001-12-01
期刊：
影响因子：
7.7
通讯作者：
Rossetti, L
中科院分区：
文献类型：
--
作者：
Wang, JL;Obici, S;Rossetti, L
在常见形式的肥胖症中，多食症、高胰岛素血症和高瘦素血症共存。在这里，我们展示了短期过度喂养快速诱导胰岛素和瘦素抵抗。在指定的饮食方案3天和7天后，测试大鼠对血浆胰岛素和瘦素浓度急性升高的生物学反应。在过度喂养3天后，对瘦素和胰岛素的代谢作用产生了严重的抵抗。在胰岛素钳夹研究期间，对照大鼠的葡萄糖产生减少了70%，过度喂养大鼠减少了28-53%。同样，瘦素输注使对照组大鼠的葡萄糖输出量增加一倍，但未能改变过度喂养动物的葡萄糖输出量。这些研究结果表明，营养过剩的反应是一个矛盾和快速崩溃的瘦素系统。这种部分失败与胰岛素抵抗的发生密切相关。
In common forms of obesity, hyperphagia, hyperinsulinemia, and hyperleptinemia coexist. Here, we demonstrate rapid induction of insulin and leptin resistance by short-term overfeeding. After 3 and 7 days on the assigned diet regimen, rats were tested for their biological responses to acute elevations in plasma insulin and leptin concentrations. Severe resistance to the metabolic effects of both leptin and insulin ensued after just 3 days of overfeeding. During the insulin clamp studies, glucose production was decreased by similar to 70% in control rats and 28-53% in overfed rats. Similarly, leptin infusion doubled the contribution of gluconeogenesis to glucose output in control rats but failed to modify gluconeogenesis in overfed animals. These findings demonstrate a paradoxical and rapid collapse of the leptin system in response to nutrient excess. This partial failure is tightly coupled with the onset of insulin resistance.