期刊
ACTA PHYSIOLOGICA
卷 220, 期 2, 页码 238-250出版社
WILEY
DOI: 10.1111/apha.12821
关键词
blood glucose; diiodothyronine; insulin response; metabolism; thyroid hormone; thyromimetic
类别
资金
- NIH [RC4 DK090849]
- CNPq [305936/2013-1]
- FAPESP [2013/05629-4, 2012/17430-5, 2010/18151-7]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [10/18151-7, 12/17430-5] Funding Source: FAPESP
AimThyroid hormones regulate metabolic response. While triiodothyronine (T3) is usually considered to be the active form of thyroid hormone, one form of diiodothyronine (3,5-T2) exerts T3-like effects on energy consumption and lipid metabolism. 3,5-T2 also improves glucose tolerance in rats and 3,5-T2 levels correlate with fasting glucose in humans. Presently, however, little is known about mechanisms of 3,5-T2 effects on glucose metabolism. Here, we set out to compare effects of T3, 3,5-T2 and another form of T2 (3,3-T2) in a mouse model of diet-induced obesity and determined effects of T3 and 3,5-T2 on markers of classical insulin sensitization to understand how diiodothyronines influence blood glucose. MethodsCell- and protein-based assays of thyroid hormone action. Assays of metabolic parameters in mice. Analysis of transcript and protein levels in different tissues by qRT-PCR and Western blot. ResultsT3 and 3,5-T2 both reduce body weight, adiposity and body temperature despite increased food intake. 3,3-T2 lacks these effects. T3 and 3,5-T2 reduce blood glucose levels, whereas 3,3-T2 worsens glucose tolerance. Neither T3 nor 3,5-T2 affects markers of insulin sensitization in skeletal muscle or white adipose tissue (WAT), but both reduce hepatic GLUT2 glucose transporter levels and glucose output. T3 and 3,5-T2 also induce expression of mitochondrial uncoupling proteins (UCPs) 3 and 1 in skeletal muscle and WAT respectively. Conclusions3,5-T2 influences glucose metabolism in a manner that is distinct from insulin sensitization and involves reductions in hepatic glucose output and changes in energy utilization.
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。
推荐
暂无数据