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C75与肥胖症药物靶点通路之间的联系。

The connections between C75 and obesity drug-target pathways.

作者信息

Kuhajda Francis P, Landree Leslie E, Ronnett Gabriele V

机构信息

Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

出版信息

Trends Pharmacol Sci. 2005 Nov;26(11):541-4. doi: 10.1016/j.tips.2005.09.002. Epub 2005 Sep 16.

Abstract

Obesity and its attendant disorders, such as Type II diabetes, have reached epidemic proportions in the USA, and their prevalence is increasing globally. C75 is a small-molecule inhibitor of fatty acid synthase (FAS) and a stimulator of carnitine palmitoyl 1 activity, which causes profound weight loss in mice. Although C75 is not a compound that is destined for human drug development, it has provided two potential pathways to target in obesity therapy: fatty acid synthesis and fatty acid oxidation. In this article, we discuss the latest data challenging the relationship between fatty acid synthase inhibition and C75-induced anorexia.

摘要

肥胖及其相关疾病,如II型糖尿病,在美国已达到流行程度,且在全球范围内其患病率正在上升。C75是脂肪酸合酶(FAS)的小分子抑制剂和肉碱棕榈酰转移酶1活性的刺激剂,可使小鼠体重显著减轻。尽管C75并非用于人类药物研发的化合物,但它为肥胖治疗提供了两条潜在的靶向途径:脂肪酸合成和脂肪酸氧化。在本文中,我们讨论了质疑脂肪酸合酶抑制与C75诱导的厌食之间关系的最新数据。

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