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FoxO Transcription Factors Are Critical Regulators of Diabetes-Related Muscle Atrophy
Journal article   Open access   Peer reviewed

FoxO Transcription Factors Are Critical Regulators of Diabetes-Related Muscle Atrophy

Brian T. O'Neill, Gourav Bhardwaj, Christie M. Penniman, Megan T. Krumpoch, Pablo A. Suarez Beltran, Katherine Klaus, Kennedy Poro, Mengyao Li, Hui Pan, Jonathan M. Dreyfuss, …
Diabetes (New York, N.Y.), Vol.68(3), pp.556-570
03/01/2019
DOI: 10.2337/db18-0416
PMCID: PMC6385751
PMID: 30523026
url
https://europepmc.org/articles/pmc6385751View
Published (Version of record) Open Access

Abstract

Insulin deficiency and uncontrolled diabetes lead to a catabolic state with decreased muscle strength, contributing to disease-related morbidity. FoxO transcription factors are suppressed by insulin and thus are key mediators of insulin action. To study their role in diabetic muscle wasting, we created mice with muscle-specific triple knockout of Fox01/3/4 and induced diabetes in these M-FoxO-TKO mice with streptozotocin (STZ). Muscle mass and myofiber area were decreased 20-30% in STZ-Diabetes mice due to increased ubiquitin-proteasome degradation and autophagy alterations, characterized by increased LC3-containing vesicles, and elevated levels of phosphorylated ULK1 and LC3-II. Both the muscle loss and markers of increased degradation/autophagy were completely prevented in STZ FoxO-TKO mice. Transcriptomic analyses revealed FoxO-dependent increases in ubiquitin-mediated proteolysis pathways in STZ-Diabetes, including regulation of Fbxo32 (Atrogin1), Trim63 (MuRF1), Bnip3L, and Gabarapl. These same genes were increased 1.4- to 3.3-fold in muscle from humans with type 1 diabetes after shortterm insulin deprivation. Thus, FoxO-regulated genes play a rate-limiting role in increased protein degradation and muscle atrophy in insulin-deficient diabetes.
Endocrinology & Metabolism Life Sciences & Biomedicine Science & Technology

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