Suppression of fat deposition for the life time with gene therapy
Suppression of fat deposition for the life time with gene therapy
复制标题
DOI：
10.1016/j.peptides.2005.03.039
复制
发表时间：
2005-08-01
期刊：
影响因子：
3
通讯作者：
Kalra, SP
中科院分区：
文献类型：
--
作者：
Boghossian, S;Lecklin, A;Kalra, SP
未消耗的能量以脂肪的形式储存在体内，脂肪增加的速度增加最终导致肥胖。肥胖会使许多疾病的风险增加数倍，并缩短寿命。瘦素（一种由脂肪细胞和下丘脑产生的肽）的中枢反馈作用的进行性缺陷导致体重增加和肥胖。本文总结了我们的实验结果表明，一个稳定的增加瘦素的可用性在下丘脑单独与瘦素基因治疗的援助，抑制脂肪增生和代谢激素几乎一生的实验室啮齿动物。因此，中枢瘦素基因治疗是一种新的方式，提供了一个可行的治疗选择，以减少脂肪库和伴随的代谢后遗症与肥胖相关的疾病。(c)2005年爱思唯尔公司All rights reserved.
Unexpended energy is stored as fat in the body and increased rate of fat accretion culminates in obesity. Obesity increases the risks of many diseases several folds and shortens life span. A progressive deficit in the central feedback effects of leptin, a peptide produced by fat cells and hypothalamus, results in increased weight gain and obesity. This article summarizes our experimental findings to show that a stable increase in leptin availability in the hypothalamus alone with the aid of leptin gene therapy suppresses fat accretion and metabolic hormones for nearly the lifetime of laboratory rodents. Consequently, central leptin gene therapy is a novel modality that offers a viable therapeutic option to reduce fat depots and attendant metabolic sequelae implicated in obesity-related illnesses. (c) 2005 Elsevier Inc. All rights reserved.