Fucoidan ameliorates diabetic skeletal muscle atrophy through PI3K/Akt pathway

• Published in: Journal of functional foods Vol. 114; p. 106076
• Main Authors: Li, Caixia, Liu, Yaping, Yang, Mingzhi, Huang, Haoyue, Tang, Lulu, Miao, Yufan, Li, Wenjie, Li, Xing
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01.03.2024; Elsevier
• Subjects: C2C12; Fucoidan; PI3K/Akt; Skeletal muscle atrophy; T2DM; Skeletal muscle atrophy; T2DM; C2C12; Fucoidan; PI3K/Akt
• ISSN: 1756-4646; 2214-9414
• DOI: 10.1016/j.jff.2024.106076

[Display omitted] •Fucoidan treatment alleviated protein metabolism disorders in T2DM rats.•Fucoidan treatment rescued diabetic skeletal muscle atrophy.•Fucoidan treatment activated the PI3K/Akt signaling pathway.•LY294002 promoted the myotubes atrophy induced by PA in C2C12 cells. It has been reported that fucoidan plays a beneficial role in type 2 diabetic mellitus (T2DM). However, it remains obscure if fucoidan has the protective effects on diabetes induced skeletal muscle atrophy. Here, we investigated the effect and mechanism of fucoidan on diabetic muscle atrophy. The results revealed that fucoidan ameliorated the general symptoms of diabetes, alleviated insulin resistance, as well as improved glucose metabolism disorders in vivo and vitro. Moreover, fucoidan also improved the atrophy of skeletal muscle by resisting the reduction of muscle fiber diameter and balance the protein anabolism and catabolism. It is worth noting that these beneficial effects of fucoidan on skeletal muscle atrophy and insulin resistance were abolished by inhibiting PI3K/Akt pathway. Taken together, fucoidan ameliorates diabetic skeletal muscle atrophy at least partially by the PI3K/Akt pathway.