The connections between C75 and obesity drug-target pathways
The connections between C75 and obesity drug-target pathways
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DOI：
10.1016/j.tips.2005.09.002
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发表时间：
2005-11-01
影响因子：
13.8
通讯作者：
Ronnett, GV
中科院分区：
文献类型：
--
作者：
Kuhajda, FP;Landree, LE;Ronnett, GV
肥胖及其伴随的疾病，如II型糖尿病，在美国已经达到流行病的比例，并且其患病率在全球范围内增加。C75是脂肪酸合成酶（FAS）的小分子抑制剂和肉毒碱棕榈酰1活性的刺激剂，其导致小鼠体重显著减轻。虽然C75不是一种用于人类药物开发的化合物，但它提供了两种潜在的肥胖治疗靶向途径：脂肪酸合成和脂肪酸氧化。在这篇文章中，我们讨论了最新的数据挑战脂肪酸合成酶抑制和C75诱导的厌食症之间的关系。
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.