Sweet Potato [Ipomoea batatas (L.) Lam. "Tainong 57"] Starch Improves Insulin Sensitivity in High-Fructose Diet-Fed Rats by Ameliorating Adipocytokine Levels, Pro-Inflammatory Status, and Insulin Signaling

  • CHEN Ya-Yen
    School of Nutrition and Health Sciences, Taipei Medical University
  • LAI Ming-Hoang
    Department of Nursing, Cardinal Tien Junior College of Healthcare and Management
  • HUNG Hsin-Yu
    School of Nutrition and Health Sciences, Taipei Medical University
  • LIU Jen-Fang
    School of Nutrition and Health Sciences, Taipei Medical University

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タイトル別名
  • Sweet Potato [<i>Ipomoea batatas</i> (L.) Lam. “Tainong 57”] Starch Improves Insulin Sensitivity in High-Fructose Diet-Fed Rats by Ameliorating Adipocytokine Levels, Pro-Inflammatory Status, and Insulin Signaling
  • Sweet Potato [Ipomoea batatas (L.) Lam. ^|^ldquo;Tainong 57^|^rdquo;] Starch Improves Insulin Sensitivity in High-Fructose Diet-Fed Rats by Ameliorating Adipocytokine Levels, Pro-Inflammatory Status, and Insulin Signaling
  • Liu, Sweet potato [Ipomoea batatas (L.) Lam. "Tainong 57"] starch improves insulin sensitivity in high-fructose diet-fed rats by ameliorating adipocytokine levels, pro-inflammatory status, and insulin signaling

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The aim of this study was to investigate the effects of low-glycemic index (GI) sweet potato starch on adipocytokines, pro-inflammatory status, and insulin signaling in the high-fructose diet-induced insulin-resistant rat. We randomly divided 24 insulin-resistant rats and 16 normal rats into two groups fed a diet containing 575 g/kg of starch: a low-GI sweet potato starch (S) or a high-GI potato starch (P). The four experimental groups were labeled as follows: insulin-resistant P (IR-P), insulin-resistant S (IR-S), normal P (N-P) and normal S (N-S). After 4 wk on the experimental diets, an intraperitoneal glucose tolerance test (IPGTT) was conducted, and the homeostasis model assessment (HOMA), adipocytokines, pro-inflammatory cytokines levels, and insulin signaling-related protein expression were measured. The homeostasis model assessment values were significantly lower in the IR-S than in the IR-P group, suggesting that insulin sensitivity was improved among sweet potato starch-fed rats. Levels of tumor necrosis factor-α, interleukin-6, resistin, and retinol binding protein-4 were significantly lower in the IR-S versus the IR-P group, indicating an improvement of pro-inflammatory status in sweet potato starch-fed rats. The sweet potato starch diet also significantly enhanced the protein expression of phospho-Tyr-insulin receptor substrate-1 and improved the translocation of glucose transporter 4 in the skeletal muscle. Our results illustrated that sweet potato starch feeding for 4 wk can improve insulin sensitivity in insulin-resistant rats, possibly by improving the adipocytokine levels, pro-inflammatory status, and insulin signaling.

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