DGAT:治疗肥胖和2型糖尿病的新靶点。

Angela Subauste, Charles F Burant
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引用次数: 28

摘要

肥胖目前是人类非常普遍的问题。过去几年在肥胖相关领域的研究取得了重大突破。甘油三酯被认为是脂肪储存多余卡路里的主要形式。甘油三酯合成的关键酶是酰基辅酶A:二酰基甘油酰基转移酶(DGAT)。最近的研究表明,缺乏这种酶的小鼠对饮食引起的肥胖有抵抗力,并增加了胰岛素和瘦素的敏感性。这些结果表明,体内抑制DGAT可能不仅是治疗肥胖的新靶点,也是治疗糖尿病的新靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
DGAT: novel therapeutic target for obesity and type 2 diabetes mellitus.

Obesity is currently an exceptionally common problem in humans. The last several years have produced a significant number of breakthroughs in obesity related areas of investigation. Triglycerides are considered the main form of storage of excess calories in fat. A key enzyme in the synthesis of triglycerides is acylCoA: diacylglycerol acyltransferase (DGAT). Recent studies have shown that mice deficient in this enzyme are resistant to diet induced obesity and have increased insulin and leptin sensitivity. These effects suggest that inhibition of DGAT in vivo may be a novel therapeutic target not only for obesity but also for diabetes.

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