Astaxanthin attenuates skeletal muscle atrophy and mitochondrial dysfunction in streptozotocin-induced diabetic rats.

Authors

Masayuki Tanaka, Miho Kanazashi, Ryosuke Nakanishi, Hiroyo Kondo, Hidemi Fujino

Published in

Biochemical and biophysical research communications. Volume 832. Pages 154374. Jul 30, 2026. Epub Jul 30, 2026.

Abstract

Diabetes mellitus (DM) induces skeletal muscle atrophy and mitochondrial dysfunction. Although antioxidant supplementation has exhibited beneficial effects on diabetic skeletal muscle, the effects of astaxanthin (AST), a potent antioxidant that protects mitochondrial function, remain unclear. We investigated whether AST supplementation attenuates DM-induced skeletal muscle alterations in streptozotocin (STZ)-induced diabetic rats. Male Wistar rats were assigned to control, DM, and DM + AST groups. DM was induced via STZ injection, and AST (100 mg/kg/day) was administered orally for 6 weeks. The plantaris muscle was analyzed for morphology, mitochondrial function, oxidative stress, inflammatory status, and signaling pathways related to protein metabolism and atrophy. Diabetic rats exhibited reductions in muscle mass and fiber cross-sectional area, decreases in mitochondrial enzyme activity and mitochondrial protein content, and increased oxidative stress. The expression of pro-inflammatory cytokines was elevated, along with markers associated with ubiquitin-proteasome system-, autophagy-, and apoptosis-related signaling. AST supplementation improved muscle mass and fiber cross-sectional area, partially restored mitochondrial enzyme activity and related protein expression, reduced oxidative stress, and attenuated inflammatory and atrophy-related signaling, without improving hyperglycemia. These findings indicate that AST attenuates DM-induced skeletal muscle atrophy and mitochondrial dysfunction in fast-twitch plantaris muscle. The protective effects of AST appear to be associated with reduced oxidative stress, attenuated inflammation, and attenuation of atrophy-related signaling rather than the restoration of anabolic signaling.

PMID:
42543059
Bibliographic data and abstract were imported from PubMed on 03 Aug 2026.

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