Iranian Journal of Diabetes and Obesity
Shahid Sadoughi University Of Medical Sciences
Sun, Oct 26, 2025
[Archive]
Volume 17, Issue 4 (12-2025)
IJDO 2025, 17(4): 0-0 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Janbozorgi M, Hosseinzadeh M, Hemati Farsani Z, Shabani M. The Effect of Exercise Training Timing on SREBP Gene Expression in Adipose Tissue of Diabetic Mice. IJDO 2025; 17 (4)
URL: http://ijdo.ssu.ac.ir/article-1-994-en.html
URL: http://ijdo.ssu.ac.ir/article-1-994-en.html
Assistant Professor, Department of Sport Sciences, Faculty of Humanities and Social Sciences, Ardakan University, Ardakan, Iran.
Abstract: (16 Views)
Objective: Sterol regulatory element-binding protein-1c (SREBP-1c) regulates lipid metabolism, and its disruption in diabetes leads to lipid accumulation, insulin resistance, and inflammation. BMAL1, a core circadian clock gene, modulates physiological rhythms. This study aimed to examine the effect of aerobic exercise timing on BMAL1 and SREBP-1c expression in adipose tissue of diabetic mice.
Materials and Methods: Thirty male mice were randomly assigned to two temporal groups: ZT3 (light phase) and ZT15 (dark phase). Within each time point, animals were divided into three subgroups: Healthy Control (HC), Diabetic Control (DC), and Diabetic + Exercise Training (TD). Diabetes was induced using a high-fat diet and streptozotocin injections. After confirmation, the TD groups performed treadmill running for eight weeks (60–80 min/day, 50–60% Vmax, 5 days/week) at their respective time points. Gene expression of BMAL1 and SREBP-1c was analyzed using Real-time PCR, and data were statistically evaluated using SPSS.
Results: Exercise during the dark phase significantly increased BMAL1 (P< 0.0001) and SREBP1 (P< 0.05) levels in the diabetic group compared to the diabetic control group. No significant differences were observed in BMAL1 or SREBP1 levels between the diabetic control group and the diabetic group with exercise during the light phase.
Conclusion: The results show that by upregulating BMAL1 and SREBP-1c in adipose tissue, evening exercise improves metabolic status in diabetic mice. These findings lay the groundwork for further translational research in humans and point to possible uses in developing time-specific exercise interventions for the management of diabetes.
Materials and Methods: Thirty male mice were randomly assigned to two temporal groups: ZT3 (light phase) and ZT15 (dark phase). Within each time point, animals were divided into three subgroups: Healthy Control (HC), Diabetic Control (DC), and Diabetic + Exercise Training (TD). Diabetes was induced using a high-fat diet and streptozotocin injections. After confirmation, the TD groups performed treadmill running for eight weeks (60–80 min/day, 50–60% Vmax, 5 days/week) at their respective time points. Gene expression of BMAL1 and SREBP-1c was analyzed using Real-time PCR, and data were statistically evaluated using SPSS.
Results: Exercise during the dark phase significantly increased BMAL1 (P< 0.0001) and SREBP1 (P< 0.05) levels in the diabetic group compared to the diabetic control group. No significant differences were observed in BMAL1 or SREBP1 levels between the diabetic control group and the diabetic group with exercise during the light phase.
Conclusion: The results show that by upregulating BMAL1 and SREBP-1c in adipose tissue, evening exercise improves metabolic status in diabetic mice. These findings lay the groundwork for further translational research in humans and point to possible uses in developing time-specific exercise interventions for the management of diabetes.
Type of Study: Research |
Subject:
Special
Received: 2025/10/26 | Accepted: 2025/12/23 | Published: 2025/12/23
Received: 2025/10/26 | Accepted: 2025/12/23 | Published: 2025/12/23
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
