The Effect of Aerobic Exercise and Berberine Chloride on the Expression of SIRT1 and AMPK Genes in Visceral Adipose Tissue of Diabetic Rats

Mitochondrial collapse caused by oxidative stress is one of the important factors of insulin resistance. The purpose of this study is to investigate the effect of aerobic exercise and berberine chloride on the indices of mitochondrial regeneration and biogenesis of visceral adipose tissue in streptozotocin-diabetic rats.

32 male Wistar rats were randomly divided into four groups (n=8): diabetes (DM), diabetes-berberine (BDM), diabetes-aerobic exercise (TDM), diabetes-aerobic exercise-berberine (TBDM). Diabetes was induced by STZ injection in male rats. Berberine chloride (30 mg/kg/day) was administered orally by gavage once a day. The exercise groups performed an incremental aerobic exercise program (10-18 m/min, 10-40 min/day, and five days/week) on a treadmill for six weeks. Gene expression levels of SIRT1 and AMPK factors in visceral adipose tissue were measured using Real time-PCR method. Data analysis was conducted using one-way analysis of variance and if significant, Tukey's post hoc test was used at a significance level of p<0.05.

Data analysis showed that there is a significant difference in the expression of SIRT1 (p<0.05) and AMPK (p<0.05) genes among the groups. Furthermore, the results showed that the expression of SIRT1 gene in the diabetes-exercise group (p<0.05) and diabetes-exercise-berberine chloride (p<0.05) had a significant increase compared to the diabetes group. Berberine chloride alone could not significantly increase SIRT1 gene expression compared to the diabetic group (p>0.05). Also, the expression of AMPK gene in diabetes-exercise (p<0.05), diabetes-berberine chloride (p<0.05) and diabetes-exercise-berberine chloride (p<0.05) groups had a significant increase compared to the diabetes group.

Based on the above findings, it is possible that the simultaneous effect of exercise and berberine chloride could inhibit oxidative stress and inflammation caused by diabetes through the AMPK-SIRT1-PPARγ pathway.