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三价铬组氨酸配合物对高脂肪饮食诱导肥胖大鼠的影响。

Impact of chromium histidinate on high fat diet induced obesity in rats.

机构信息

Department of Animal Nutrition, Faculty of Veterinary Science, Firat University, 23119 Elazig, Turkey.

出版信息

Nutr Metab (Lond). 2011 May 3;8:28. doi: 10.1186/1743-7075-8-28.

Abstract

BACKGROUND

Chromium (Cr) is an essential trace element that has garnered interest for use as a weight loss aid, but its molecular mechanism in obesity is not clear. In this study, an attempt has been made to investigate the effects of chromium histidinate (CrHis) on glucose transporter-2 (GLUT-2), nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), nuclear factor-kappa B (NF-κB p65) and the oxidative stress marker 4-hydroxynonenal adducts (HNE) expressions in liver of rats fed high fat diet (HFD).

METHODS

Male Wistar rats (n = 40, 8 wk-old) were divided into four groups. Group I was fed a standard diet (12% of calories as fat); Group II was fed a standard diet and supplemented with 110 μg CrHis/kg BW/d; Group III was fed a HFD (40% of calories as fat); Group IV was fed HFD and supplemented with 110 μg CrHis/kg BW/d.

RESULTS

Rats fed HFD possessed greater serum insulin (40 vs.33 pmol/L) and glucose (158 vs. 143 mg/dL) concentration and less liver Cr (44 vs.82 μg/g) concentration than rats fed the control diet. However, rats supplemented with CrHis had greater liver Cr and serum insulin and lower glucose concentration in rats fed HFD (P < 0.05). The hepatic nuclear factor-kappa B (NF-κB p65) and HNE were increased in high fat group compared to control group, but reduced by the CrHis administration (P < 0.05). The levels of hepatic Nrf2 and HO-1 were increased by supplementation of CrHis (P < 0.05).

CONCLUSION

These findings demonstrate that supplementation of CrHis is protective against obesity, at least in part, through Nrf2-mediated induction of HO-1 in rats fed high fat diet.

摘要

背景

铬(Cr)是一种必需的微量元素,因其具有减肥辅助作用而受到关注,但它在肥胖中的分子机制尚不清楚。本研究试图探讨铬组氨酸(CrHis)对高脂肪饮食(HFD)喂养大鼠肝脏葡萄糖转运蛋白-2(GLUT-2)、核因子红细胞 2 相关因子 2(Nrf2)、血红素加氧酶-1(HO-1)、核因子-κB(NF-κB p65)和氧化应激标志物 4-羟基壬烯醛加合物(HNE)表达的影响。

方法

雄性 Wistar 大鼠(n=40,8 周龄)分为 4 组。第 1 组喂食标准饮食(12%的热量来自脂肪);第 2 组喂食标准饮食并补充 110μg CrHis/kg BW/d;第 3 组喂食 HFD(40%的热量来自脂肪);第 4 组喂食 HFD 并补充 110μg CrHis/kg BW/d。

结果

与对照组相比,HFD 喂养大鼠的血清胰岛素(40 vs.33 pmol/L)和血糖(158 vs.143 mg/dL)浓度更高,肝脏 Cr(44 vs.82 μg/g)浓度更低。然而,CrHis 补充组可使 HFD 喂养大鼠的肝脏 Cr、血清胰岛素和血糖浓度降低(P < 0.05)。与对照组相比,高脂肪组肝核因子-κB(NF-κB p65)和 HNE 增加,但 CrHis 给药可减少其表达(P < 0.05)。CrHis 补充可增加肝 Nrf2 和 HO-1 水平(P < 0.05)。

结论

这些发现表明,CrHis 补充剂通过 Nrf2 介导的 HO-1 诱导对 HFD 喂养大鼠具有保护作用,至少部分是通过 Nrf2 介导的 HO-1 诱导来实现的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20d1/3094204/827d9f3c6d8a/1743-7075-8-28-1.jpg

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