An adipocyte-specific defect in oxidative phosphorylation increases systemic energy expenditure and protects against diet-induced obesity in mouse models - Choi, Min Jeong; Jung, Saet-Byel; Lee, Seong Eun; Kang, Seul Gi; Lee, Ju Hee; Ryu, Min Jeong; Chung, Hyo Kyun; Chang, Joon Young; Kim, Yong Kyung; Hong, Hyun Jung; Kim, Hail; Kim, Hyun Jin; et al. (Diabetologia, 2020)
Keywords: Adipocytes; Adipocytes - metabolism; Adipocytes - pathology; Adipose tissue; Animal models; Animals; Antibiotics; Body weight gain; Cell Cycle Proteins - genetics; Cell Cycle Proteins - metabolism; Cellular stress response; Diabetes; Diet, High-Fat; Disease Models, Animal; Doxycycline; Energy balance; Energy expenditure; Energy metabolism; Energy Metabolism - genetics; Fibroblast growth factors; Glucose tolerance; High fat diet; Homeostasis; Human Physiology; Insulin; Insulin resistance; Internal Medicine; Male; Medicine; Medicine & Public Health; Metabolic Diseases; Metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Obese; Mitochondria; Mitokine; Obesity; Obesity - genetics; Obesity - metabolism; Obesity - prevention & control; Organ Specificity - genetics; Oxidative Phosphorylation; Phenotypes; Phosphorylation; Protein folding; Ribonucleic acid; RNA; Insulin resistance; Energy metabolism; Mitochondria; Adipose tissue; Mitokine