{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T15:16:35Z","timestamp":1791645395396,"version":"4.3.4"},"reference-count":50,"publisher":"Bioscientifica","issue":"1","funder":[{"name":"Japan Society for the Promotion of Science, Japan Association for Diabetes Education and Care","award":["24K23776, 22K17773, 23K10839, 23K28017"],"award-info":[{"award-number":["24K23776, 22K17773, 23K10839, 23K28017"]}]}],"content-domain":{"domain":["journals.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,1,1]]},"abstract":"<jats:p>Diabetes is an increasingly prevalent global disease and is often accompanied by sarcopenia, particularly in older adults. While insulin resistance is a well-known contributor to muscle loss in diabetes, the role of glucose signaling in diabetic skeletal muscle atrophy, particularly under insulin-deficient conditions, remains poorly understood. This study aimed to elucidate the pathophysiological role of the carbohydrate-responsive element-binding protein (ChREBP), a glucose-sensing transcription factor encoded by the Chrebp gene in mice, in diabetic sarcopenia by generating Chrebp-deficient, insulin-deficient Ins2Akita\/+ mice. We evaluated Chrebp+\/+, Chrebp\u2212\/\u2212, Ins2Akita\/+\/Chrebp+\/+, and Ins2Akita\/+\/Chrebp\u2212\/\u2212 mice for muscle strength, endurance, survival, body composition, and muscle histology. Skeletal muscles were analyzed for gene expressions related to anabolic and catabolic pathways. We found that Ins2Akita\/+\/Chrebp\u2212\/\u2212 mice exhibited significant reductions in body weight, grip strength, survival, and skeletal muscle mass \u2013 particularly in the tibialis anterior, soleus, gastrocnemius, and quadriceps \u2013 compared to Ins2Akita\/+ controls, despite similar hyperglycemia. Histological analysis revealed a smaller mean muscle fiber size and reduced cross-sectional area of type 2A and 2B fibers, without changes in fiber-type composition. Furthermore, Igf-1 expression was suppressed, while the atrophy marker Fbxo32\/Atrogin-1 was upregulated. These findings demonstrate that Chrebp deletion exacerbates muscle atrophy and frailty in insulin-deficient mice, underscoring a key role for ChREBP-mediated glucose signaling in maintaining muscle mass under diabetic conditions. The Ins2Akita\/+\/Chrebp\u2212\/\u2212 model provides a valuable platform for exploring diabetic sarcopenia mechanisms and potential therapeutic targets.<\/jats:p>","DOI":"10.1530\/joe-25-0257","type":"journal-article","created":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T12:05:29Z","timestamp":1767960329000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-5","source":"Crossref","is-referenced-by-count":1,"title":["ChREBP deficiency aggravates diabetic sarcopenia by disrupting glucose signaling: a novel mouse model of muscle 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