A Genetic Model to Study the Contribution of Brown and Brite Adipocytes to Metabolism
Copyright policy )A Genetic Model to Study the Contribution of Brown and Brite Adipocytes to Metabolism
UCP1-dependent thermogenesis is studied to define new strategies to ameliorate obesity and type 2 diabetes; however, animal models are mostly limited to germline mutations of UCP1, which can effect adaptive changes in UCP1-independent pathways. We develop an inducible mouse model for the sequential ablation of UCP1+ brown and brite/beige adipocytes in adult mice. We demonstrate that activated brown adipocytes can increase systemic energy expenditure (EE) by 30%, while the contribution of brite/beige UCP1+ cells is <5%. Notably, UCP1+ adipocytes do not contribute to circulating FGF21 levels, either at room temperature or after cold exposure. We demonstrate that the FGF21-mediated effects on EE and glucose homeostasis are partially dependent on the presence of UCP1+ cells, while the effect on weight loss is not. In conclusion, acute UCP1+ cell deletion may be a useful model to study the impact of brown and brite/beige adipocytes on metabolism.
Cell Reports, 30 (10)
ISSN:2666-3864
ISSN:2211-1247
- ETH Zurich Switzerland
Models, Genetic, QH301-705.5, Temperature, Fibroblast Growth Factors, Mice, Inbred C57BL, Adipocytes, Brown, Animals, Adipocytes, Beige, Biology (General), Energy Metabolism, Gene Deletion, Uncoupling Protein 1
Models, Genetic, QH301-705.5, Temperature, Fibroblast Growth Factors, Mice, Inbred C57BL, Adipocytes, Brown, Animals, Adipocytes, Beige, Biology (General), Energy Metabolism, Gene Deletion, Uncoupling Protein 1
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