不利影响
过氧化物酶体增殖物激活受体
罗格列酮
更安全的
核受体
2型糖尿病
细胞生物学
信号转导
疾病
胰岛素受体
生物信息学
过氧化物酶体
糖尿病
药理学
受体
医学
生物
内分泌学
内科学
胰岛素抵抗
转录因子
计算机科学
生物化学
基因
计算机安全
作者
Maryam Ahmadian,Jae Myoung Suh,Nasun Hah,Christopher Liddle,Annette R. Atkins,Michael Downes,Ronald M. Evans
出处
期刊:Nature Medicine
[Springer Nature]
日期:2013-05-01
卷期号:19 (5): 557-566
被引量:1528
摘要
Thiazolidinediones (TZDs) are potent insulin sensitizers that act through the nuclear receptor peroxisome proliferator-activated receptor-γ (PPARγ) and are highly effective oral medications for type 2 diabetes. However, their unique benefits are shadowed by the risk for fluid retention, weight gain, bone loss and congestive heart failure. This raises the question as to whether it is possible to build a safer generation of PPARγ-specific drugs that evoke fewer side effects while preserving insulin-sensitizing potential. Recent studies that have supported the continuing physiologic and therapeutic relevance of the PPARγ pathway also provide opportunities to develop newer classes of molecules that reduce or eliminate adverse effects. This review highlights key advances in understanding PPARγ signaling in energy homeostasis and metabolic disease and also provides new explanations for adverse events linked to TZD-based therapy.
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