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有氧运动训练和维生素 D 补充对 2 型糖尿病大鼠血糖指标和脂肪组织基因表达的影响。

Effects of aerobic training and vitamin D supplementation on glycemic indices and adipose tissue gene expression in type 2 diabetic rats.

机构信息

Department of Exercise Physiology, Faculty of Sport Sciences, Razi University, P.O. Box. 6714414971, Kermanshah, Iran.

Department of Biology, Faculty of Science, Razi University, Kermanshah, Iran.

出版信息

Sci Rep. 2023 Jun 23;13(1):10218. doi: 10.1038/s41598-023-37489-z.

Abstract

Type 2 diabetes mellitus (T2DM) is a progressive metabolic disorder mainly caused by overweight and obesity that accumulates pro-inflammatory factors in adipose tissue. Studies have confirmed the efficacy of exercise and vitamin D supplementation in preventing, controlling, and treating diabetes. While, reduced physical activity and vitamin D deficiency are related to increased adiposity, blood glucose level, insulin concentration, and insulin resistance. This study purposed to investigate the effect of 8-week aerobic training with vitamin D supplementation on the expression of AMPK, PGC-1α, and UCP-1 genes expression in the visceral adipose tissue of obese rats with T2DM. In this experimental study, fifty male Wistar rats were divided into 5 groups (n = 10): aerobic training and vitamin D supplementation (AT + Vit D), aerobic training (5 days/week for 8 weeks; AT), vitamin D supplementation (Vit D), diabetic control (C) and NC (Non-Diabetic Control). AT + Vit D and AT groups practiced an 8-week aerobic training, 5 days a week. Vit D and AT + Vit D groups receive 5000 IU of vitamin D by injection once a week while AT and C received sesame oil. After blood sampling, visceral fat was taken to measure AMPK, PGC-1α, and UCP1 gene expression. Data were statistically analyzed by One-way ANOVA and paired sample t-test at a significance level of p < 0.05. Based on our results BW, BMI, WC, visceral fat, insulin, glucose, and HOMA-IR were significantly lower in the AT + Vit D, AT, and Vit D groups compared with the C group (p < 0.01). Furthermore, AT + Vit D, AT, and Vit D upregulated AMPK, PGC-1α, and UCP1 gene expression compared to the C. Based on the results compared to AT and Vit D, AT + Vit D significantly upregulated AMPK (p = 0.004; p = 0.001), PGC-1α (p = 0.010; p = 0.001), and UCP1 (p = 0.032; p = 0.001) gene expression, respectively. Also, AT induced more significant upregulations in the AMPK (p = 0.001), PGC-1α (p = 0.001), and UCP1 gene expression (p = 0.001) than Vit D. Vitamin D supplementation enhanced the beneficial effects of aerobic training on BW, BMI, WC, visceral fat, insulin, glucose, and HOMA-IR in diabetic rats. We also observed that separate AT or Vit D upregulated the gene expression of AMPK, PGC-1α, and UCP1 however, combined AT + Vit D upregulated AMPK, PGC-1α, and UCP1 more significantly. These results suggested that combining aerobic training and vitamin D supplementation exerted incremental effects on the gene expressions related to adipose tissue in animal models of diabetes.

摘要

2 型糖尿病(T2DM)是一种主要由超重和肥胖引起的进行性代谢紊乱,会在脂肪组织中积累促炎因子。研究已经证实,运动和维生素 D 补充剂在预防、控制和治疗糖尿病方面是有效的。然而,体力活动减少和维生素 D 缺乏与肥胖、血糖水平、胰岛素浓度和胰岛素抵抗增加有关。本研究旨在探讨 8 周有氧运动联合维生素 D 补充对 T2DM 肥胖大鼠内脏脂肪组织中 AMPK、PGC-1α 和 UCP-1 基因表达的影响。

在这项实验研究中,将 50 只雄性 Wistar 大鼠分为 5 组(n=10):有氧运动联合维生素 D 补充(AT+Vit D)、有氧运动(每周 5 天,持续 8 周;AT)、维生素 D 补充(Vit D)、糖尿病对照组(C)和非糖尿病对照组(NC)。AT+Vit D 和 AT 组每周进行 5 天的有氧运动。Vit D 和 AT+Vit D 组每周接受 5000IU 维生素 D 注射,而 AT 和 C 组接受芝麻油。采血后,取内脏脂肪测量 AMPK、PGC-1α 和 UCP1 基因表达。数据采用单因素方差分析和配对样本 t 检验进行统计学分析,显著性水平为 p<0.05。

根据我们的结果,与 C 组相比,AT+Vit D、AT 和 Vit D 组的 BW、BMI、WC、内脏脂肪、胰岛素、葡萄糖和 HOMA-IR 显著降低(p<0.01)。此外,与 C 组相比,AT+Vit D、AT 和 Vit D 组 AMPK、PGC-1α 和 UCP1 基因表达均上调。与 AT 和 Vit D 相比,AT+Vit D 显著上调 AMPK(p=0.004;p=0.001)、PGC-1α(p=0.010;p=0.001)和 UCP1(p=0.032;p=0.001)基因表达。此外,AT 诱导的 AMPK(p=0.001)、PGC-1α(p=0.001)和 UCP1 基因表达(p=0.001)上调更为显著。维生素 D 补充增强了有氧运动对糖尿病大鼠 BW、BMI、WC、内脏脂肪、胰岛素、葡萄糖和 HOMA-IR 的有益作用。我们还观察到,单独的 AT 或 Vit D 上调了 AMPK、PGC-1α 和 UCP1 的基因表达,但联合的 AT+Vit D 上调更为显著。

这些结果表明,在糖尿病动物模型中,有氧运动联合维生素 D 补充对与脂肪组织相关的基因表达具有叠加效应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/889f/10290097/5e7174b0ce50/41598_2023_37489_Fig1_HTML.jpg

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