Autophagy in Myf5+ progenitors regulates energy and glucose homeostasis through control of brown fat and skeletal muscle development
| Autor: | Rajat Singh, Srabani Sahu, Claire C. Bastie, Nuria Martinez-Lopez, Diana Athonvarangkul, Jeffrey E. Pessin, Gary J. Schwartz, Luisa Coletto, Haihong Zong |
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| Rok vydání: | 2013 |
| Předmět: |
medicine.medical_specialty
animal structures Adipose tissue White adipose tissue Biology Carbohydrate metabolism Autophagy-Related Protein 7 Biochemistry Mice Adipose Tissue Brown Internal medicine Brown adipose tissue Autophagy Genetics medicine Animals Homeostasis Glucose homeostasis Muscle Skeletal Molecular Biology Stem Cells Fatty Acids Scientific Reports brown fat Skeletal muscle Cell Differentiation musculoskeletal system QP Glucose Endocrinology medicine.anatomical_structure MYF5 Myogenic Regulatory Factor 5 Energy Metabolism Microtubule-Associated Proteins Myf5+ progenitors |
| Zdroj: | EMBO Reports |
| ISSN: | 1469-3178 1469-221X |
| Popis: | Autophagy in Myf5+ progenitors regulates energy and glucose homeostasis through control of brown fat and skeletal muscle development Atg7 deletion in Myf5+ progenitors blocks autophagy in brown adipose tissue and muscle, affecting their differentiation and function. Knockout mice have higher body temperatures and glucose intolerance, underscoring the importance of autophagy in these processes. Macroautophagy (MA) regulates cellular quality control and energy balance. For example, loss of MA in aP2-positive adipocytes converts white adipose tissue (WAT) into brown adipose tissue (BAT)-like, enhancing BAT function and thereby insulin sensitivity. However, whether MA regulates early BAT development is unknown. We report that deleting Atg7 in myogenic Myf5+ progenitors inhibits MA in Myf5-cell-derived BAT and muscle. Knock out (KO) mice have defective BAT differentiation and function. Surprisingly, their body temperature is higher due to WAT lipolysis-driven increases in fatty acid oxidation in ‘Beige' cells in inguinal WAT, BAT and muscle. KO mice also present impaired muscle differentiation, reduced muscle mass and glucose intolerance. Our studies show that ATG7 in Myf5+ progenitors is required to maintain energy and glucose homeostasis through effects on BAT and muscle development. Decreased MA in myogenic progenitors with age and/or overnutrition might contribute to the metabolic defects and sarcopenia observed in these conditions. |
| Databáze: | OpenAIRE |
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