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提取物通过增强高脂肪饮食诱导肥胖小鼠 AMPK 的激活来减轻胰岛素抵抗。

Extract Reduces Insulin Resistance by Enhancing AMPK Activation in High-Fat Diet-Induced Obese Mice.

机构信息

Department of Biochemistry, School of Biological Sciences, Chungbuk National University, Cheongju 28644, Korea.

Mushroom Research Division, National Institute of Horticultural and Herbal Science, RDA Eumseong, Chungbuk 27709, Korea.

出版信息

Nutrients. 2020 Oct 30;12(11):3338. doi: 10.3390/nu12113338.

Abstract

is used widely in oriental medicine to treat obesity and metabolic diseases. Bioactive substances extracted from have been shown to ameliorate dyslipidemia, insulin resistance, and type 2 diabetes in mice via multiple 5' AMP-activated protein kinase (AMPK)-mediated mechanisms; however, further studies are required to elucidate the anti-obesity effects of in vivo. In this study, we demonstrated that 3% extract powder (GEP) can be used to prevent obesity and insulin resistance in a mouse model. C57BL/6 mice were provided with a normal diet (ND) or a high-fat diet (HFD) supplemented with 1, 3, or 5% GEP for 12 weeks and the effect of GEP on body weight, liver, adipose tissue, adipokines, insulin and glucose tolerance (ITT and GTT), glucose uptake, glucose-metabolism related proteins, and lipogenesis related genes was examined. GEP administration was found to reduce weight gain in the liver and fat tissues of the mice. In addition, serum parameters were significantly lower in the 3% and 5% GEP mice groups than in those fed a HFD alone, whereas adiponectin levels were significantly higher. We also observed that GEP improved glucose metabolism, reduced lipid accumulation in the liver, and reduced adipocyte size. These effects may have been mediated by enhanced AMPK activation, which attenuated the transcription and translation of lipogenic genes such as fatty acid synthase (FAS), stearoyl-CoA desaturase 1 (SCD1), and sterol regulatory element-binding protein-1c (SREBP1c). Moreover, AMP-activated protein kinase (AMPK) activation increased acetyl-CoA carboxylase (ACC), insulin receptor (IR), IR substrate 1 (IRS1), and Akt protein expression and activation, as well as glucose transporter type 1/4 (GLUT1/4) protein production, thereby improving insulin sensitivity and glucose metabolism. Together, these findings demonstrate that may effectively prevent obesity and suppress obesity-induced insulin resistance via AMPK activation.

摘要

在东方医学中被广泛用于治疗肥胖症和代谢疾病。从 中提取的生物活性物质已被证明通过多种 5' 腺苷酸活化蛋白激酶 (AMPK) 介导的机制改善了小鼠的血脂异常、胰岛素抵抗和 2 型糖尿病;然而,还需要进一步的研究来阐明 在体内的抗肥胖作用。在这项研究中,我们证明了 3% 提取物粉末 (GEP) 可用于预防肥胖症和胰岛素抵抗的小鼠模型。C57BL/6 小鼠给予正常饮食 (ND) 或高脂肪饮食 (HFD) ,并补充 1%、3% 或 5% 的 GEP 12 周,研究 GEP 对体重、肝脏、脂肪组织、脂肪因子、胰岛素和葡萄糖耐量 (ITT 和 GTT)、葡萄糖摄取、葡萄糖代谢相关蛋白和脂肪生成相关基因的影响。发现 GEP 可减少小鼠肝脏和脂肪组织的体重增加。此外,与单独给予 HFD 的小鼠相比,3% 和 5% GEP 组的血清参数显著降低,而脂联素水平显著升高。我们还观察到 GEP 改善了葡萄糖代谢,减少了肝脏的脂质积累,并减少了脂肪细胞的大小。这些作用可能是通过增强 AMPK 激活介导的,AMPK 激活减弱了脂肪酸合酶 (FAS)、硬脂酰辅酶 A 去饱和酶 1 (SCD1) 和固醇调节元件结合蛋白-1c (SREBP1c) 等脂肪生成基因的转录和翻译。此外,AMPK 激活增加了乙酰辅酶 A 羧化酶 (ACC)、胰岛素受体 (IR)、IR 底物 1 (IRS1) 和 Akt 蛋白表达和激活,以及葡萄糖转运蛋白 1/4 (GLUT1/4) 蛋白的产生,从而提高了胰岛素敏感性和葡萄糖代谢。总之,这些发现表明 可能通过 AMPK 激活有效预防肥胖症和抑制肥胖引起的胰岛素抵抗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04d5/7693844/edcebba8d56b/nutrients-12-03338-g002.jpg

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