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首页> 外文期刊>Nature >Leptin reverses insulin resistance and diabetes mellitus in mice with congenital lipodystrophy
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Leptin reverses insulin resistance and diabetes mellitus in mice with congenital lipodystrophy

机译：瘦素逆转先天性脂肪营养不良小鼠的胰岛素抵抗和糖尿病

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Congenital generalized lipodystrophy (CGL) is a rare autosomal recessive disorder characterized by a paucity of adipose (fat) tissue which is evident at birth and is accompanied by a severe resistance to insulin, leading to hyperinsulinaemia, hyperglycaemia and enlarged fatty liver. We have developed a mouse model that mimics these features of CGL: the syndrome occurs in transgenic mice expressing a truncated version of a nuclear protein known as nSREBP-1c (for sterol-regulatory-element-binding protein-1c) under the control of the adipose-specific aP2 enhancer. Adipose tissue from these mice was markedly deficient in messenger RNAs encoding several fat-specific proteins, including leptin, a fat-derived hormone that regulates food intake and energy metabolism. Here we show that insulin resistance in our lipody-strophic mice can be overcome by a continuous systemic infusion of low doses of recombinant leptin, an effect that is not mimicked by chronic food restriction. Our results support the idea that leptin modulates insulin sensitivity and glucose disposal independently of its effect on food intake, and that leptin deficiency accounts for the insulin resistance found in CGL.
机译：先天性泛发性脂肪营养不良（CGL）是一种罕见的常染色体隐性遗传疾病，其特征是缺乏脂肪（脂肪）组织，这种组织在出生时就很明显，并且伴有严重的胰岛素抵抗，导致高胰岛素血症，高血糖症和肥大的脂肪肝。我们已经开发出了一种模仿CGL这些特征的小鼠模型：该综合征发生在表达被称为nSREBP-1c（用于固醇调节元素结合蛋白-1c）的核蛋白的截短版本的转基因小鼠中。脂肪特异性aP2增强剂。这些小鼠的脂肪组织明显缺乏编码几种脂肪特异性蛋白质的信使RNA，包括瘦素，瘦素是一种脂肪衍生的激素，可调节食物摄入和能量代谢。在这里，我们表明，通过连续全身性输注低剂量的重组瘦素可以克服我们的脂肪营养不良小鼠的胰岛素抵抗，这种作用不能被长期的食物限制所模仿。我们的研究结果支持了瘦素独立于其对食物摄入的影响而调节胰岛素敏感性和葡萄糖处置的想法，并且瘦素缺乏是CGL中胰岛素抵抗的原因。

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