Why the study?
Diabetic heart disease is characterized by myocardial alterations, prompting investigation into the effects of exercise training on oxidative phosphorylation-related genes in the diabetic heart.
Does 12-week exercise training improve oxidative phosphorylation-related gene expression in a murine model of diabetic cardiomyopathy?
Does 12-week exercise training improve oxidative phosphorylation-related gene expression in a murine model of diabetic cardiomyopathy?
Exercise training upregulates oxidative phosphorylation-related genes in the diabetic murine heart, suggesting a molecular mechanism for improved cardiac function.
Should not yet change practice in diabetic cardiomyopathy; hypothesis-generating for oxidative phosphorylation modulation via exercise.
Diabetic heart disease is marked by structural, functional, and molecular alterations in the myocardium. We investigated the effects of exercise training on oxidative phosphorylation-related genes in the diabetic heart. Male mice C57BL/6JNarl (n = 24) were randomly divided into three equal groups: STZ-induced diabetic group with 12-week exercise training (DM-EX); diabetic group (DM); a non-diabetic control group. After completion of exercise training, samples from the soleus and heart tissues were collected from all the mice. Out of eight mouse samples from the DM and DM-EX, two left ventricles from either group were randomly selected and processed for RNA extraction and microarray analysis. Exercise training changed the expression of 517 genes (P < 0.05); 380 upregulated,137 downregulated. Enrichment analysis depicted that apoptosis, diabetic cardiomyopathy, and oxidative phosphorylation were most significantly regulated. Pathway analysis revealed that exercise training upregulated 17 key oxidative phosphorylation genes, including complex I (Ndufa13, Ndufb4, Ndufb8, Ndufb9, Ndufc1, Ndufc2, Ndufs4, Ndufv2), complex III (Uqcrfs1, Uqcrh), complex IV (Cox5A, Cox7A, Cox17), and complex V (Atp5e, Atp5g3, Atp5k, Atp5l). Exercise training amplifies the gene expression concerned with oxidative phosphorylation in the diabetic heart, showing its potential to modulate molecular pathways that influence cardiac functions and improve the diabetic heart. Not applicable.
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Shah et al. (2026) studied this question.
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