Skeletal Muscle Redox Imbalance and Fibrosis in rats fed short- and long-term sucrose-rich diet: preventive effects of Chia Seed (Salvia hispanica L.).

Authors

Paola G Illesca, María Eugenia Oliva, Noelia Villafañe, Paola Ingaramo, María Eugenia D'Alessandro

Published in

Molecular and cellular endocrinology. Pages 112921. Oct 06, 2026. Epub Oct 06, 2026.

Abstract

The present study aimed to explore the involvement of oxidative stress (OS) and fibrosis in the metabolic impairment of skeletal muscle (SkM) induced in the short (3 weeks) and long term (15 weeks) by a sucrose-rich diet (SRD) and the effects of dietary chia seed as a preventive therapeutic strategy. Male Wistar rats were fed with a reference diet (RD), an SRD or an SRD whit whole chia seed incorporated as the source of dietary fat (SRD+Chia) for two time periods 3 and 15 weeks. Results showed that OS and fibrosis contribute from the early stages of SRD-induced SkM impairment and that chia administration exerts time-dependent protective effects. At long-term, chia prevented the increase in visceral adiposity and preserve gastrocnemius muscle mass lost induced by the SRD. At both time points chia prevented dyslipidemia, hyperuricemia, lipid peroxidation, and the increase in blood pressure, while preserve glucose serum level at 15 weeks. In SkM, short-term intervention preserved reduced glutathione (GSH) levels, whereas in long-term chia partially prevented lipid accumulation and markedly improved antioxidant defenses by maintaining GSH levels and glutathione peroxidase activity while increasing glutathione reductase activity. Moreover, preventive chia administration attenuated both early and late SkM collagen deposition, accompanied by reduced TGF-β mRNA expression. This work provides novel evidence supporting the early involvement of OS and extracellular matrix remodeling in SkM deterioration. Moreover, it expands current knowledge of the preventive potential of chia seeds against SkM alterations associated with metabolic disease.

PMID:
42833511
Bibliographic data and abstract were imported from PubMed on 06 Oct 2026.

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