4.8 Article

Long-Term Cold Adaptation Does Not Require FGF21 or UCP1

期刊

CELL METABOLISM
卷 26, 期 2, 页码 437-+

出版社

CELL PRESS
DOI: 10.1016/j.cmet.2017.07.016

关键词

-

资金

  1. German Center for Diabetes Research (DZD)
  2. Alexander von Humboldt Foundation
  3. Helmholtz Alliance ICEMED
  4. Helmholtz Initiative on Personalized Medicine iMed by Helmholtz Association
  5. Helmholtz cross-program topic Metabolic Dysfunction

向作者/读者索取更多资源

Brown adipose tissue (BAT)-dependent thermogenesis and its suggested augmenting hormone, FGF21, are potential therapeutic targets in current obesity and diabetes research. Here, we studied the role of UCP1 and FGF21 for metabolic homeostasis in the cold and dissected underlying molecular mechanisms using UCP1-FGF21 double-knockout mice. We report that neither UCP1 nor FGF21, nor even compensatory increases of FGF21 serum levels in UCP1 knockout mice, are required for defense of body temperature or for maintenance of energy metabolism and body weight. Remarkably, cold-induced browning of inguinal white adipose tissue (iWAT) is FGF21 independent. Global RNA sequencing reveals major changes in response to UCP1- but not FGF21-ablation in BAT, iWAT, and muscle. Markers of mitochondrial failure and inflammation are observed in BAT, but in particular the enhanced metabolic reprogramming in iWAT supports the thermogenic role of UCP1 and excludes an important thermogenic role of endogenous FGF21 in normal cold acclimation.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.8
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据