FoxO Transcription Factors Are Critical Regulators of Diabetes-Related Muscle Atrophy
Open accessAbstract
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 FoxO1/3/4 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 short-term insulin deprivation. Thus, FoxO-regulated genes play a rate-limiting role in increased protein degradation and muscle atrophy in insulin-deficient diabetes.
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FoxO1,3,4 are transcription factors downstream of the IGF1/insulin-Akt pathway, and their inhibition completely spares muscle loss and force drop in fasting, hind limb suspension, immobilization, diabetes, and glucocorticoids treatment.
“FoxO1,3,4 are transcription factors downstream the IGF1/insulin-Akt pathway (Fig. 1) and their inhibition completely spares muscle loss and force drop in fasting, hind limb suspension, immobilization, diabetes, and glucocorticoids treatment3,57,63,64.”
From Mechanisms of muscle atrophy and hypertrophy: implications in health and disease (2021) · cites this paper as [63]
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- Authors
- O’Neill, B. T., Bhardwaj, G., Penniman, C. M., Krumpoch, M. T., Suarez Beltran, P. A., Klaus, K., Poro, K., Li, M., Pan, H., Dreyfuss, J. M., Nair, K. S., & Kahn, C. R.
- Affiliations
- Fraternal Order of Eagles Diabetes Research Center and Division of Endocrinology and Metabolism, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA
- University of Iowa (US)
- Joslin Diabetes Center (US)
- Mayo Clinic (US)
- Boston University (US)
- Corresponding author
- Kahn, C. Ronald
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2018-12-06
- Volume
- 68
- Issue
- 3
- Pages
- 556-570
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- PMC
- PMC6385751
- OpenAlex
- W2807617425
- Cited by
- 167
- References
- 59
- Citations by year
- 2026: 13 · 2025: 17 · 2024: 24 · 2023: 26 · 2022: 25 · 2021: 26 · 2020: 27 · 2019: 8
- FWCI
- 5.43
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Diabetes (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01-DK-031036, R01-DK-033201, R01-DK-41973, U24-DK-100469, K08-DK-100543, R03-DK-112003, UL1-TR-000135, P30-DK-36836)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › FOXO transcription factor regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- FOXO transcription factors, muscle atrophy, type 1 diabetes, insulin deficiency, ubiquitin-proteasome degradation, autophagy, atrogin-1, MuRF1, BNIP3L, streptozotocin-induced diabetes, muscle-specific knockout mice, protein degradation
- MeSH terms
- Forkhead Box Protein O1, Forkhead Box Protein O3, Amino Acids, Animals, Autophagy, Diabetes Mellitus, Experimental, Female, Humans, Insulin, Lysosomes, Male, Muscle Proteins, Muscular Atrophy, Phosphorylation, DNA, Complementary, Mice, Knockout, Muscle, Skeletal, Cell Cycle Proteins, Reverse Transcriptase Polymerase Chain Reaction, Mice, Forkhead Transcription Factors, Proteolysis
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