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脂肪生成在以色列沙鼠(肥胖沙鼠)肥胖和糖尿病发展中的作用

The role of lipogenesis in the development of obesity and diabetes in Israeli sand rats (Psammomys obesus).

作者信息

Lewandowski P A, Cameron-Smith D, Jackson C J, Kultys E R, Collier G R

机构信息

School of Nutrition and Public Health, Deakin University, Geelong, Victoria 3217, Australia.

出版信息

J Nutr. 1998 Nov;128(11):1984-8. doi: 10.1093/jn/128.11.1984.

DOI:10.1093/jn/128.11.1984
PMID:9808653
Abstract

Obesity and diabetes in Israeli sand rats, Psammomys obesus, occur with the sequential transition of animals from normal insulin sensitivity to impaired insulin sensitivity, accompanied by increased adiposity, prior to insulin resistance and obesity, in a manner similar to susceptible human populations. The current study was designed to examine the role of de novo lipid synthesis in the development of excessive weight gain in P. obesus. Sand rats were classified at 12 wk of age into three groups: A, normoglycemic normoinsulinemic; B, normoglycemic hyperinsulinemic; C, hyperglycemic hyperinsulinemic, based on glucose and insulin responses in fed sand rats. Body weight, liver weight, white adipose tissue (WAT) mass and food intake were significantly elevated in Group C compared to Group A (P < 0.05). Lipogenic rate was measured by the amount of 3H incorporated into subscapular brown adipose tissue (BAT), epidiymal WAT and liver per hour, from sand rats with and without access to food. No difference in lipogenic rate was found between the groups in BAT, indicating that this tissue is of minor importance in whole body lipogenesis in P. obesus. In the WAT there was a greater lipogenic rate with the development of obesity and hyperinsulinemia (Group B vs. Group A) but no difference in the liver. However, the onset of hyperglycemia (Group C) further stimulated WAT lipogenesis and initiated increased hepatic lipogenesis, both of which contributed to the pre-existing obesity. This study suggests that elevated lipogenesis is not the primary cause of obesity in P. obesus, as lipogenic rate only markedly increases after obesity is already present in hyperglycemic animals.

摘要

以色列沙鼠(肥尾沙鼠,Psammomys obesus)的肥胖和糖尿病发生过程中,动物会从正常胰岛素敏感性依次转变为胰岛素敏感性受损,在出现胰岛素抵抗和肥胖之前伴有肥胖增加,其方式与易感人群相似。本研究旨在探讨从头合成脂质在肥尾沙鼠体重过度增加过程中的作用。根据喂食沙鼠的葡萄糖和胰岛素反应,将12周龄的沙鼠分为三组:A组,血糖正常胰岛素正常;B组,血糖正常胰岛素高;C组,血糖高胰岛素高。与A组相比,C组的体重、肝脏重量、白色脂肪组织(WAT)质量和食物摄入量显著升高(P < 0.05)。通过每小时掺入肩胛下棕色脂肪组织(BAT)、附睾WAT和肝脏中的3H量来测量脂质生成率,实验对象为有食物供应和无食物供应的沙鼠。BAT组之间的脂质生成率没有差异,这表明该组织在肥尾沙鼠全身脂质生成中不太重要。在WAT中,随着肥胖和高胰岛素血症的发展(B组与A组相比)脂质生成率更高,但肝脏中没有差异。然而,高血糖的出现(C组)进一步刺激了WAT脂质生成并引发肝脏脂质生成增加,这两者都导致了先前已存在的肥胖。本研究表明,脂质生成增加不是肥尾沙鼠肥胖的主要原因,因为只有在高血糖动物已经出现肥胖后脂质生成率才会显著增加。

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