TNP [N2-(m-Trifluorobenzyl), N6-(p-nitrobenzyl)purine] ameliorates diet induced obesity and insulin resistance via inhibition of the IP6K1 pathway
详细信息 查看全文
- 作者：Sarbani Ghoshal1 ; Qingzhang Zhu1 ; Alice Asteian2 ; 5 ; Hua Lin2 ; Haifei Xu3 ; Glen Ernst4 ; James C. Barrow4 ; Baoji Xu3 ; Michael D. Cameron2 ; Theodore M. Kamenecka2 ; Anutosh Chakraborty1 ; achakrab@scripps.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：IP6K ; Inositol pyrophosphate ; Obesity ; Energy expenditure ; Diabetes ; Akt
- 刊名：Molecular Metabolism
- 出版年：2016
- 出版时间：October 2016
- 年：2016
- 卷：5
- 期：10
- 页码：903-917
- 全文大小：2516 K
文摘
- •
Pharmacologic inhibition of IP6K by TNP, at the onset of high fat feeding, decelerates initiation of DIO and insulin resistance in mice.
- •
TNP, when treated to DIO mice, promotes weight loss and restores metabolic homeostasis.
- •
TNP does not reduce high fat diet induced weight gain in IP6K1-KO mice.
- •
TNP promotes insulin sensitivity by stimulating Akt activity, whereas it reduces body weight primarily by enhancing thermogenic energy expenditure.
- •
Long-term TNP treatment does not display deleterious side effects.