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实验模型中的热量限制、体脂与衰老

Caloric restriction, body fat and ageing in experimental models.

作者信息

Das M, Gabriely I, Barzilai N

机构信息

Institute for Ageing Research, Diabetes Research and Training Center, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

出版信息

Obes Rev. 2004 Feb;5(1):13-9. doi: 10.1111/j.1467-789x.2004.00115.x.

Abstract

Caloric restriction in animal models delays many age-related pathological conditions. Ageing rats have characteristically increased body weight, fat mass and a specific body fat distribution. This report will focus on the potential cause-effect relationship between increased fat mass and accelerated ageing. In humans, increased fat mass (obesity), and in particular increases in abdominal obesity as a result of deposition of visceral fat, are associated with the metabolic syndrome of ageing. This syndrome is associated with hyperinsulinaemia, dyslipidaemia, type 2 diabetes mellitus, atherosclerosis, hypercoagulability and hypertension. Fat tissue, however, plays a major role by secreting multiple metabolically active factors, which are potentially responsible for the development of insulin resistance. This article will review various experimental models (in animals) used to prevent insulin resistance of ageing by decreasing fat mass, and in particular, decreasing visceral fat. We suggest that this decrease in fat mass and its beneficial repercussions observed in ageing animal models may apply also to human ageing and its related pathology.

摘要

动物模型中的热量限制可延缓许多与年龄相关的病理状况。衰老的大鼠具有体重增加、脂肪量增加以及特定体脂分布的特征。本报告将聚焦于脂肪量增加与加速衰老之间潜在的因果关系。在人类中,脂肪量增加(肥胖),尤其是由于内脏脂肪沉积导致的腹部肥胖增加,与衰老的代谢综合征相关。该综合征与高胰岛素血症、血脂异常、2型糖尿病、动脉粥样硬化、高凝状态和高血压有关。然而,脂肪组织通过分泌多种具有代谢活性的因子发挥主要作用,这些因子可能是胰岛素抵抗发展的原因。本文将综述用于通过减少脂肪量,特别是减少内脏脂肪来预防衰老相关胰岛素抵抗的各种(动物)实验模型。我们认为,在衰老动物模型中观察到的脂肪量减少及其有益影响可能也适用于人类衰老及其相关病理。

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