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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2015.12
- 수록면
- 1,037 - 1,043 (7page)
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The TAZ activator 2-butyl-5-methyl-6-(pyridine-3-yl)-3- [2'-(1H-tetrazole-5-yl)-biphenyl-4-ylmethyl]-3H-imidazo[4,5- b]pyridine] (TM-25659) inhibits adipocyte differentiation by interacting with peroxisome proliferator-activated receptor gamma. 1 TM-25659 was previously shown to decrease weight gain in a high fat (HF) diet-induced obesity (DIO) mouse model. However, the fundamental mechanisms underlying the effects of TM-25659 remain unknown.
Therefore, we investigated the effects of TM-25659 on skeletal muscle functions in C2 myotubes and C57BL/6J mice.
We studied the molecular mechanisms underlying the contribution of TM-25659 to palmitate (PA)-induced insulin resistance in C2 myotubes. TM-25659 improved PAinduced insulin resistance and inflammation in C2 myotubes.
In addition, TM-25659 increased FGF21 mRNA expression, protein levels, and FGF21 secretion in C2 myotubes via activation of GCN2 pathways (GCN2-phosphoeIF2α- ATF4 and FGF21). This beneficial effect of TM-25659 was diminished by FGF21 siRNA. C57BL/6J mice were fed a HF diet for 30 weeks. The HF-diet group was randomly divided into two groups for the next 14 days: the HF-diet and HF-diet + TM-25659 groups. The HF diet + TM-25659- treated mice showed improvements in their fasting blood glucose levels, insulin sensitivity, insulin-stimulated Akt phosphorylation, and inflammation, but neither body weight nor food intake was affected. The HF diet + TM- 25659-treated mice also exhibited increased expression of both FGF21 mRNA and protein. These data indicate thatTM-25659 may be beneficial for treating insulin resistance by inducing FGF21 in models of PA-induced insulin resistance and HF diet-induced insulin resistance.
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참고문헌 (24)
참고문헌 신청
Anthony, T. G. / 2004 / Preservation of liver protein synthesis during dietary leucine deprivation occurs at the expense of skeletal muscle mass in mice deleted for eIF2kinase GCN2 / J. Biol. Chem 279:36553~36561
Badman, M. K. / 2007 / Hepatic fibroblast growth factor 21is regulated by PPAR alpha and is a key mediator of hepatic lipid metabolism in ketotic states / Cell Metab 5:426~437
De Sousa-Coelho, A. L. / 2013 / FGF21 mediates the lipid metabolism response to amino acid starvation / J. Lipid Res 54:1786~1797
Fisher, F. M. / 2010 / Obesity is a fibroblast growth factor 21(FGF21)-resistant state / Diabetes 59:2781~2789
Ge, X. / 2012 / Metabolic actions of FGF21 : molecular mechanisms and therapeutic implications / Acta Pharmaceutica Sinica B 2:350~357
Badman, M. K. / 2007 / Hepatic fibroblast growth factor 21is regulated by PPAR alpha and is a key mediator of hepatic lipid metabolism in ketotic states / Cell Metab 5:426~437
De Sousa-Coelho, A. L. / 2013 / FGF21 mediates the lipid metabolism response to amino acid starvation / J. Lipid Res 54:1786~1797
Fisher, F. M. / 2010 / Obesity is a fibroblast growth factor 21(FGF21)-resistant state / Diabetes 59:2781~2789
Ge, X. / 2012 / Metabolic actions of FGF21 : molecular mechanisms and therapeutic implications / Acta Pharmaceutica Sinica B 2:350~357
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