Exercise training benefits pancreatic islet by modulating the insulin-like growth factor 1/phosphatidylinositol 3-kinase/protein kinase B pathway.

IF 4.6 3区医学 Q1 ENDOCRINOLOGY & METABOLISM

World Journal of Diabetes Pub Date : 2025-05-15 DOI:10.4239/wjd.v16.i5.101447

Ya-Wen Wu, Chu-Yan Wu, Feng Lin, Jun-Ying Wu

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引用次数: 0

Abstract

Background: Diabetes is characterized by insulin resistance as well as impaired insulin production, with β-cell dysfunction playing a critical role in disease progression. Exercise is known to improve insulin sensitivity, but its effects on pancreatic islet quality and function remain poorly understood. This work hypothesized that swimming training enhances glycemic control and insulin secretion by upregulating the insulin-like growth factor 1 (IGF-1)/phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway in streptozotocin (STZ)-induced diabetic rats.

Aim: To investigate the effects of swimming on pancreatic islet quality and function in STZ-induced diabetic rats via the IGF-1/PI3K/AKT pathway.

Methods: Twenty-six Sprague-Dawley rats were grouped into diabetic and control groups, with each group further split into exercise and sedentary subgroups. Diabetic rats were induced with STZ. The exercise groups underwent swimming training for 60 minutes/day, 5 days/week, for 8 weeks. Body weight, food intake, blood glucose, insulin, lipids, and muscle glycogen were measured. Pancreatic islet morphology and the protein expression levels of IGF-1, PI3K, and AKT were analyzed. Data were analyzed using two-way repeated-measure ANOVA, followed by Tukey's post-hoc test.

Results: Exercise training significantly improved body weight [diabetic exercise group (D-Ex): 390.66 ± 50.14 g vs diabetic sedentary group (D-Sed): 315.89 ± 50.12 g, P < 0.05], reduced blood glucose (D-Ex: 12.21 ± 4.43 mmol/L vs D-Sed: 17.79 ± 2.05 mmol/L, P < 0.05), and increased insulin levels (D-Ex: 53.50 ± 15.31 pmol/L vs D-Sed: 25.31 ± 10.23 pmol/L, P < 0.05) in diabetic rats. It also enhanced islet morphology, increased IGF-1 expression, and activated the PI3K/AKT pathway (P < 0.05). In-vitro experiments confirmed that IGF-1 positively regulated insulin expression and inhibited β-cell apoptosis via the PI3K/AKT pathway.

Conclusion: Exercise training improves pancreatic islet quality and function in diabetic rats by modulating the IGF-1/PI3K/AKT pathway, highlighting its therapeutic potential for diabetes management.

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运动训练通过调节胰岛素样生长因子1/磷脂酰肌醇3-激酶/蛋白激酶B通路对胰岛有益。

背景：糖尿病以胰岛素抵抗和胰岛素生成受损为特征，β细胞功能障碍在疾病进展中起关键作用。众所周知，运动可以改善胰岛素敏感性，但它对胰岛质量和功能的影响仍知之甚少。本研究假设游泳训练通过上调链脲佐菌素（STZ）诱导的糖尿病大鼠胰岛素样生长因子1 (IGF-1)/磷脂酰肌醇3-激酶/蛋白激酶B （PI3K/AKT）通路，促进血糖控制和胰岛素分泌。目的：探讨游泳通过IGF-1/PI3K/AKT通路对stz诱导的糖尿病大鼠胰岛质量和功能的影响。方法：将26只Sprague-Dawley大鼠分为糖尿病组和对照组，每组又分为运动组和久坐组。采用STZ诱导糖尿病大鼠。运动组进行游泳训练，每天60分钟，每周5天，共8周。测量体重、食物摄入量、血糖、胰岛素、血脂和肌糖原。分析各组胰岛形态及IGF-1、PI3K、AKT蛋白表达水平。数据分析采用双向重复测量方差分析，随后进行Tukey事后检验。结果：运动训练显著改善糖尿病大鼠体重[糖尿病运动组（D-Ex）： 390.66±50.14 g，糖尿病久坐组（D-Sed）： 315.89±50.12 g, P < 0.05]，降低血糖（D-Ex: 12.21±4.43 mmol/L vs D-Sed: 17.79±2.05 mmol/L, P < 0.05），升高胰岛素水平（D-Ex: 53.50±15.31 pmol/L vs D-Sed: 25.31±10.23 pmol/L, P < 0.05）。它还能增强胰岛形态，增加IGF-1表达，激活PI3K/AKT通路（P < 0.05）。体外实验证实IGF-1通过PI3K/AKT通路正向调节胰岛素表达，抑制β-细胞凋亡。结论：运动训练通过调节IGF-1/PI3K/AKT通路改善糖尿病大鼠胰岛质量和功能，突出其治疗糖尿病的潜力。

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来源期刊

World Journal of Diabetes ENDOCRINOLOGY & METABOLISM-

自引率

2.40%

发文量

909

期刊介绍： The WJD is a high-quality, peer reviewed, open-access journal. The primary task of WJD is to rapidly publish high-quality original articles, reviews, editorials, and case reports in the field of diabetes. In order to promote productive academic communication, the peer review process for the WJD is transparent; to this end, all published manuscripts are accompanied by the anonymized reviewers’ comments as well as the authors’ responses. The primary aims of the WJD are to improve diagnostic, therapeutic and preventive modalities and the skills of clinicians and to guide clinical practice in diabetes. Scope: Diabetes Complications, Experimental Diabetes Mellitus, Type 1 Diabetes Mellitus, Type 2 Diabetes Mellitus, Diabetes, Gestational, Diabetic Angiopathies, Diabetic Cardiomyopathies, Diabetic Coma, Diabetic Ketoacidosis, Diabetic Nephropathies, Diabetic Neuropathies, Donohue Syndrome, Fetal Macrosomia, and Prediabetic State.