Activated apoptotic and anti-survival effects on rat hearts with fructose induced metabolic syndrome

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题名:	Activated apoptotic and anti-survival effects on rat hearts with fructose induced metabolic syndrome
作者:	鄭秀敏;Cheng, Shiu-Min;黃志揚;HUANG, CHIH-YANG;李信達;Lee, Shin-Da
贡献者:	生物科技學系
关键词:	Apoptosis;Fas receptor;Fructose;Heart;Metabolic syndrome;TNF-alpha
日期:	2014-03
上传时间:	2014-07-03 07:41:11 (UTC+0)
摘要:	Consumption of fructose has been linked to the development of metabolic syndrome, whereas the cardiomyopathic changes and cardiac apoptosis of dietary high-fructose intake have not yet been clarified. The purpose of this study was to evaluate the effects of high-fructose on cardiac apoptotic and survival pathways. Thirty-two Wistar rats were randomly divided into a control group (CON), which received a standard chow diet, and a fructose-induced metabolic syndrome group (FIMS), which received a 50% fructose-content diet for 13 weeks. Histopathological analysis, TUNEL assays and Western blotting were performed on the excised hearts from both groups. The blood pressure, glucose, insulin, triglyceride and cholesterol levels were significantly increased in the FIMS group, compared with the CON group. The abnormal myocardial architecture, enlarged interstitial space and increased cardiac TUNEL-positive apoptotic cells were observed in the FIMS group. The TNF-α, TNF receptor 1, Fas ligand, Fas receptor, FADD, and activated caspase-3 and 8 protein levels (Fas pathway) and the Bax, Bak, Bax/Bcl-2, Bak/Bcl-xL, cytosolic cytochrome c, and activated caspase-3 and nine protein levels (mitochondria pathway) were increased in the FIMS group compared with those in the CON group. The IGFI, IGFI-R, p-PI3K, p-Akt, Bcl-2 and Bcl-xL protein levels (survival pathway) were all significantly decreased in the FIMS group compared with those in the CON group. High-fructose intake elevated blood pressure and glucose levels; moreover, high-fructose diet activated cardiac Fas-dependent and mitochondria-dependent apoptotic pathways and suppressed the survival pathway, which might provide one possible mechanism for developing heart failure in patients with metabolic syndrome.
關聯:	CELL BIOCHEMISTRY AND FUNCTION,32(2),133–141.
显示于类别:	[生物科技學系] 期刊論文

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