缺乏白色脂肪的a - zip /F-1小鼠:了解脂肪萎缩性糖尿病的模型。

M L Reitman, O Gavrilova
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引用次数: 51

摘要

A-ZIP/F-1小鼠几乎缺乏所有白色脂肪组织。与脂肪组织普遍缺乏的人类一样,a - zip /F-1小鼠也会患上严重的胰岛素抵抗型糖尿病。我们研究了A-ZIP/F-1小鼠的生理机能。它们对禁食的适应以其快速和利用冬眠状态来最大限度地减少能量需求而闻名。脂肪组织移植逆转了小鼠的代谢表现,表明脂肪组织的缺乏是胰岛素抵抗的原因。瘦素替代在逆转A-ZIP/F-1小鼠的糖尿病方面不是很有效,这与aP2-SREBP-lc小鼠的疗效形成对比。
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A-ZIP/F-1 mice lacking white fat: a model for understanding lipoatrophic diabetes.

The A-ZIP/F-1 mouse is lacking virtually all white adipose tissue. Like humans with extensive deficiencies of adipose tissue, the A-ZIP/F-1 mice develop a severe form of insulin resistant diabetes. We have studied the physiology of the A-ZIP/F-1 mice. Their adaptation to fasting is notable for its rapidity and the use of torpor, a hibernation-like state, to minimize energy needs. Transplantation of adipose tissue reversed the metabolic manifestations in the mice, demonstrating that the lack of adipose tissue is the cause of the insulin resistance. Leptin replacement is not very effective in reversing the diabetes of the A-ZIP/F-1 mice, which contrasts with its efficacy in the aP2-SREBP-lc mouse.

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Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis. Role of energy charge and AMP-activated protein kinase in adipocytes in the control of body fat stores. Role of glucocorticoids in the physiopathology of excessive fat deposition and insulin resistance. Fat storage in pancreas and in insulin-sensitive tissues in pathogenesis of type 2 diabetes. Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases.
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