Fructose induced neurogenic hypertension mediated by overactivation of p38 MAPK to impair insulin signaling transduction caused central insulin resistance

Pei Wen Cheng, Yu Te Lin, Wen Yu Ho, Pei Jung Lu, Hsin Hung Chen, Chi Cheng Lai, Gwo Ching Sun, Tung Chen Yeh, Michael Hsiao, Ching Jiunn Tseng, Chun Peng Liu

研究成果: Article同行評審

9 引文 斯高帕斯(Scopus)

摘要

Type 2 diabetes are at a high risk of complications related to hypertension, and reports have indicated that insulin levels may be associated with blood pressure (BP). Fructose intake has recently been reported to promote insulin resistance and superoxide formation. The aim of this study is to investigate whether fructose intake can enhance superoxide generation and impair insulin signaling in the NTS and subsequently elevate BP in rats with fructose-induced hypertension. Treatment with fructose for 4 weeks increased the BP, serum fasting insulin, glucose, homeostatic model assessment-insulin resistance, and triglyceride levels and reduced the serum direct high-density lipoprotein level in the fructose group. The Tempol treatment recovered the fructose-induced decrease in nitric oxide production in the NTS. Immunoblotting and immunofluorescence analyses further showed that fructose increased the p38- and fructose-induced phosphorylation of insulin receptor substrate 1 (IRS1S307) and suppressed AktS473 and neuronal nitric oxide synthase phosphorylation. Similarly, fructose was able to impair insulin sensitivity and increase insulin levels in the NTS. Fructose intake also increased the production of superoxide in the NTS. The results of this study suggest that fructose might induce central insulin resistance and elevate BP by enhancing superoxide production and activating p38 phosphorylation in the NTS.

原文English
頁(從 - 到)298-307
頁數10
期刊Free Radical Biology and Medicine
112
DOIs
出版狀態Published - 2017 十一月

All Science Journal Classification (ASJC) codes

  • 生物化學
  • 生理學(醫學)

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