Effects of Resistance Training Combined with Saffron Extract on PGC-1α and PGC-1β Gene Expression in the Soleus Muscle of Diabetic Rats

Document Type : Original Article

Authors

1 Department of Sport Sciences, Faculty of Literature and Humanities, Lorestan University, Khorramabad, Iran,

2 Department of Exercise Physiology, Faculty of Sport Sciences, Razi University

Abstract

Background and Objective: Type 2 diabetes mellitus (T2DM) is one of the most common metabolic disorders, characterized by insulin resistance and mitochondrial dysfunction. Reduced expression of PGC-1α and PGC-1β in diabetic skeletal muscle has been associated with decreased oxidative capacity, impaired glucose utilization, and increased insulin resistance. These proteins are key regulators of mitochondrial biogenesis and energy metabolism. Evidence suggests that resistance training and herbal compounds, such as saffron extract, can modulate the expression of these proteins via common pathways, particularly AMPK. This study aimed to examine the effects of resistance training combined with saffron extract on PGC-1α and PGC-1β expression in the soleus muscle of T2DM rats.
Materials and Methods: Thirty male Sprague-Dawley rats with streptozotocin-induced T2DM were randomly assigned to five groups: control (C), diabetic (D), diabetic+resistance training (DT), diabetic+saffron (DS), and diabetic+resistance training+saffron (DTS). The resistance protocol involved six weeks of ladder climbing with weights attached to the tail. Saffron extract was administered daily by gavage at 25 mg/kg body weight. Protein expression levels of PGC-1α and PGC-1β were measured using ELISA.
Results: PGC-1α expression was significantly higher in DT, DS, and DTS compared with the D group (P<0.05), with the greatest increase in DTS. PGC-1β expression showed only a slight, non-significant elevation in the intervention groups relative to D.
Conclusion: Resistance training and saffron extract, particularly in combination, exert synergistic effects on upregulating PGC-1α expression, which may enhance mitochondrial function and energy metabolism in T2DM. In contrast, PGC-1β exhibited no significant response, likely due to lower sensitivity to physiological or pharmacological stimuli. These findings suggest this combined strategy as a complementary approach for managing T2DM-related metabolic dysfunctions.

Keywords

Main Subjects