Dietary inner bran fraction of rice attenuates skeletal muscle proteolysis in rats: insights from plasma metabolomic profiling.

Authors

Miyu Kamimura, Saki Shimamoto, Kohta Hirao, Ayumi Katafuchi, Shozo Tomonaga, Mana Kawaguchi, Kiriko Nakamura, Yoko Yamauchi, Yoshikazu Fujita, Akira Ohtsuka, Daichi Ijiri

Published in

The British journal of nutrition. Pages 1-12. Sep 29, 2026. Epub Sep 29, 2026.

Abstract

In the present study, we aimed to investigate the effects of the consumption of the inner bran fraction of rice (IBFR) on the skeletal muscle of rats. Although the IBFR-containing diet did not affect the growth of the rats, it increased soleus muscle weight by suppressing skeletal muscle proteolysis along with reduced muscle atrophy F-box (Atrogin-1/MAFbx) mRNA expression. Next, to ascertain whether the anti-proteolytic effects of IBFR on skeletal muscle derive from hydrophilic or hydrophobic components, the effects of consuming either aqueous or hexane extracts (HE) of the IBFR were investigated in rats fed a protein-deficient (PD) diet. Feeding the rats the PD diet reduced skeletal muscle weight and increased muscle protein degradation and the mRNA expression of Atrogin-1/MAFbx and forkhead boxO 1 (FoxO1) in the soleus muscle. However, feeding rats the aqueous extract (AE) alleviated the PD diet-induced protein degradation, whereas supplementation with the HE had no effect. A plasma metabolomic analysis showed that AE supplementation ameliorated the metabolic disturbances caused by the PD diet, with partial restoration of the levels of glutathione- and polyamine-related metabolites that may have contributed to the reduction in skeletal muscle proteolysis. A peptidomic analysis indicated that AE contained peptides with the potential to exert these beneficial effects. These results suggest that hydrophilic compounds in IBFR reduced the mRNA expression of Atrogin-1/MAFbx and FoxO1, potentially through modulation of glutathione and polyamine metabolism, causing a reduction in muscle protein degradation in rat skeletal muscle. In addition, AE-derived peptides may partially contribute to these effects.

PMID:
42806936
Bibliographic data and abstract were imported from PubMed on 29 Sep 2026.

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