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Abstract: (293 Views)
Introduction: Sports activity increases PGC1α and Nrf2, the regulatory factors of mitochondrial biogenesis. This paper aims to study the impact of two-month sodium citrate supplementation with Moderate-Intensity Continuous Training (MICT) on PGC-1α and Nrf2 expression in diabetic rats.
Methods: Forty-five three-month-old male Wistar rats were haphazardly relegated to one of five equal groups(N=9): (1) healthy; (2) diabetic; (3) diabetes + exercise (DE); (4) diabetes+ supplementation (DS); and (5) diabetic + exercise + supplementation (DSE) and matched according to their weights. After induction, exercises began on a treadmill for 8 weeks, five days a week. The MICT protocol ran at 70% of its maximum speed for 36 minutes. The rats were sodium-citrate-supplemented at 15 mmol/L by drinking water for two months. PGC-1α and Nrf2 expression were measured through Western blotting in the soleus muscle. The data were analyzed using a univariate analysis of variance (ANOVA) and the Tukey post hoc test. Cohen’s D effect size (ES) was calculated to compare the groups.
Results: The results showed that induction of diabetes has significantly reduced the expression of PGC-1α (p< 0.001; ES=1.36) and Nrf2 (p<0.088; ES=0.24), while exercise has increased PGC-1α expression (p<0.001;ES=0.68). MICT activity/sodium citrate supplementation significantly increased the expression of PGC-1α in male diabetic rats. However, sodium citrate supplementation alone or in combination with MICT appears to have no obvious advantage over Nrf2 expression.
Conclusions: MICT activity and sodium citrate supplementation by increasing PGC-1α expression can be considered therapeutic strategies for diabetic patients. However, to increase Nrf2 expression, it is necessary to study different exercise intensities and doses of sodium citrate supplementation.
Methods: Forty-five three-month-old male Wistar rats were haphazardly relegated to one of five equal groups(N=9): (1) healthy; (2) diabetic; (3) diabetes + exercise (DE); (4) diabetes+ supplementation (DS); and (5) diabetic + exercise + supplementation (DSE) and matched according to their weights. After induction, exercises began on a treadmill for 8 weeks, five days a week. The MICT protocol ran at 70% of its maximum speed for 36 minutes. The rats were sodium-citrate-supplemented at 15 mmol/L by drinking water for two months. PGC-1α and Nrf2 expression were measured through Western blotting in the soleus muscle. The data were analyzed using a univariate analysis of variance (ANOVA) and the Tukey post hoc test. Cohen’s D effect size (ES) was calculated to compare the groups.
Results: The results showed that induction of diabetes has significantly reduced the expression of PGC-1α (p< 0.001; ES=1.36) and Nrf2 (p<0.088; ES=0.24), while exercise has increased PGC-1α expression (p<0.001;ES=0.68). MICT activity/sodium citrate supplementation significantly increased the expression of PGC-1α in male diabetic rats. However, sodium citrate supplementation alone or in combination with MICT appears to have no obvious advantage over Nrf2 expression.
Conclusions: MICT activity and sodium citrate supplementation by increasing PGC-1α expression can be considered therapeutic strategies for diabetic patients. However, to increase Nrf2 expression, it is necessary to study different exercise intensities and doses of sodium citrate supplementation.
Type of Manuscript: Experimental research article |
Subject:
Musculoskeletal Physiology/Pharmacology
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