# Effects of exercise training on oxidative phosphorylation-related genes in a diabetic heart via microarray analysis

## TL;DR

Exercise training in diabetic mice increases genes related to energy production in the heart, potentially improving heart function.

## Contribution

The study identifies specific oxidative phosphorylation genes upregulated by exercise in diabetic hearts using microarray analysis.

## Key findings

- Exercise training altered 517 genes in diabetic hearts, with 380 upregulated and 137 downregulated.
- Key oxidative phosphorylation genes, including complexes I, III, IV, and V, were upregulated by exercise training.
- Enrichment analysis showed significant regulation of apoptosis, diabetic cardiomyopathy, and oxidative phosphorylation pathways.

## Abstract

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.