进食诱导性肥胖是否需要高胰岛素血症？
Is hyperinsulinemia required to develop overeating-induced obesity?
机构信息
Department of Medicine, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029-6574, USA.
出版信息
Cell Metab. 2012 Dec 5;16(6):691-2. doi: 10.1016/j.cmet.2012.11.009.
Abstract
Type 2 diabetes is characterized by insulin resistance, and the hyperinsulinemia commonly observed in patients is thought to be a compensatory response. Yet it has been difficult to disentangle cause and effect. Mehran et al. (2012) provide genetic evidence that a reduction of insulin secretion prevents high-fat feeding-induced obesity.
摘要
2 型糖尿病的特征是胰岛素抵抗，而患者中常见的高胰岛素血症被认为是一种代偿性反应。然而，要理清因果关系一直很困难。Mehran 等人（2012 年）提供了遗传证据，表明胰岛素分泌减少可预防高脂肪喂养引起的肥胖。
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本文引用的文献
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Brain insulin controls adipose tissue lipolysis and lipogenesis.脑胰岛素控制脂肪组织的脂肪分解和脂肪生成。
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