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肉桂提取物可预防由高果糖饮食诱导的胰岛素抵抗。

Cinnamon extract prevents the insulin resistance induced by a high-fructose diet.

作者信息

Qin B, Nagasaki M, Ren M, Bajotto G, Oshida Y, Sato Y

机构信息

Department of Sports Medicine, Graduate School of Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan.

出版信息

Horm Metab Res. 2004 Feb;36(2):119-25. doi: 10.1055/s-2004-814223.

Abstract

The aim of this study was to determine whether cinnamon extract (CE) would improve the glucose utilization in normal male Wistar rats fed a high-fructose diet (HFD) for three weeks with or without CE added to the drinking water (300 mg/kg/day). In vivo glucose utilization was measured by the euglycemic clamp technique. Further analyses on the possible changes in insulin signaling occurring in skeletal muscle were performed afterwards by Western blotting. At 3 mU/kg/min insulin infusions, the decreased glucose infusion rate (GIR) in HFD-fed rats (60 % of controls, p < 0.01) was improved by CE administration to the same level of controls (normal chow diet) and the improving effect of CE on the GIR of HFD-fed rats was blocked by approximately 50 % by N-monometyl-L-arginine. The same tendency was found during the 30 mU/kg/min insulin infusions. There were no differences in skeletal muscle insulin receptor (IR)-beta, IR substrate (IRS)-1, or phosphatidylinositol (PI) 3-kinase protein content in any groups. However, the muscular insulin-stimulated IR-beta and IRS-1 tyrosine phosphorylation levels and IRS-1 associated with PI 3-kinase in HFD-fed rats were only 70 +/- 9 %, 76 +/- 5 %, and 72 +/- 6 % of controls (p < 0.05), respectively, and these decreases were significantly improved by CE treatment. These results suggest that early CE administration to HFD-fed rats would prevent the development of insulin resistance at least in part by enhancing insulin signaling and possibly via the NO pathway in skeletal muscle.

摘要

本研究的目的是确定肉桂提取物(CE)是否会改善正常雄性Wistar大鼠的葡萄糖利用情况。这些大鼠被喂食高果糖饮食(HFD)三周,饮用水中添加或不添加CE(300毫克/千克/天)。通过正常血糖钳夹技术测量体内葡萄糖利用率。随后通过蛋白质印迹法对骨骼肌中胰岛素信号可能发生的变化进行进一步分析。在以3 mU/千克/分钟的速度输注胰岛素时,喂食HFD的大鼠中降低的葡萄糖输注速率(GIR)(对照组的60%,p<0.01)通过给予CE提高到了与对照组(正常普通饮食)相同的水平,并且N-单甲基-L-精氨酸使CE对喂食HFD大鼠GIR的改善作用大约阻断了50%。在以30 mU/千克/分钟的速度输注胰岛素期间也发现了相同的趋势。任何组的骨骼肌胰岛素受体(IR)-β、胰岛素受体底物(IRS)-1或磷脂酰肌醇(PI)3激酶蛋白含量均无差异。然而,喂食HFD的大鼠中肌肉胰岛素刺激的IR-β和IRS-1酪氨酸磷酸化水平以及与PI 3激酶相关的IRS-1分别仅为对照组的70±9%、76±5%和72±6%(p<0.05),并且这些降低通过CE治疗得到了显著改善。这些结果表明,对喂食HFD的大鼠早期给予CE至少部分地通过增强胰岛素信号传导并可能通过骨骼肌中的NO途径来预防胰岛素抵抗的发展。

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