Journal
ENDOCRINOLOGY
Volume 154, Issue 10, Pages 3652-3659Publisher
OXFORD UNIV PRESS INC
DOI: 10.1210/en.2013-1113
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Funding
- Canadian Institute of Health Research (CIHR) [MOP-81148, MOP-93707]
- Eliot Phillipson Clinician Scientist Training Program
- Banting and Best Diabetes Centre
- Canadian Liver Foundation
- Canadian Diabetes Association (CDA)
- CIHR-Frederick Banting and Charles Best Canada
- Comprehensive Research Experience for Medical Students
- CDA Doctoral Student Research Award
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The growing prevalence of obesity and diabetes necessitate a better understanding of the role of adipocyte biology in metabolism. Increasingly, erythropoietin (EPO) has been shown to have extraerythropoietic and cytoprotective roles. Exogenous administration has recently been shown to have beneficial effects on obesity and diabetes in mouse models and EPO can modulate adipogenesis and insulin signaling in 3T3-L1 adipocytes. However, its physiological role in adipocytes has not been identified. Using male and female mice with adipose tissue-specific knockdown of the EPO receptor, we determine that adipocyte EPO signaling is not essential for the maintenance of energy homeostasis or glucose metabolism. Adipose tissue-specific disruption of EPO receptor did not alter adipose tissue expansion, adipocyte morphology, insulin resistance, inflammation, or angiogenesis in vivo. In contrast to the pharmacological effects of EPO, we demonstrate that EPO signaling at physiological levels is not essential for adipose tissue regulation of metabolism.
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