Exercise reverses diabetes-induced microRNA dysregulation in white adipose tissue.

Authors

Mahboobeh Yeganeh-Hajahmadi, Mohammad-Mojtaba Farazi, Saeideh Jafarinejad-Farsangi, Maryamossadat Mirtajaddini-Goki, Yasmin Moosavi-Said

Published in

Irish journal of medical science. Jul 13, 2026. Epub Jul 13, 2026.

Abstract

Type 1 diabetes mellitus (T1DM) alters microRNA (miRNA) expression in key metabolic tissues. The effects of different exercise modalities on miRNA expression in white adipose tissue (WAT) of the T1DM rat model remain largely unexplored.
This exploratory preclinical study investigated the effects of eight weeks of moderate-intensity endurance training (MIET) and high-intensity interval training (HIIT) on the expression of miR-29a and miR-126 in the WAT of the T1DM rat model.
Fifty-four male Wistar rats were randomly assigned to six groups (n = 7 in healthy and n = 11 in diabetic groups): Control, MIET, HIIT, T1DM, T1DM + MIET, and T1DM + HIIT. Diabetes was induced by a single injection of STZ (60 mg/kg).
T1DM upregulated miR-29a (15-fold, p < 0.001) and miR-126 (fourfold, p < 0.001) compared to the control. Both MIET and HIIT completely normalized miR-29a expression in diabetic rats (p < 0.001). Furthermore, both exercise interventions profoundly suppressed miR-126 expression to levels significantly below those of the T1DM group (p < 0.001). Both interventions reduced fasting blood glucose, with MIET showing a greater effect (p < 0.001).
Both MIET and HIIT normalized diabetes-induced dysregulation of miR-29a and miR-126 in WAT. These changes were associated with improved glycemic control, identifying these miRNAs as candidate responders to exercise modality in T1DM. The observed association between exercise intensity and glucose-lowering effects generates hypotheses for future mechanistic studies but does not establish causality. This exploratory study provides a candidate-based foundation for further research.

PMID:
42440197
Bibliographic data and abstract were imported from PubMed on 13 Jul 2026.

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