Disrupted erythropoietin signalling promotes obesity and alters hypothalamus proopiomelanocortin production

Ruifeng Teng, Oksana Gavrilova, Norio Suzuki, Tatyana Chanturiya, Daniel Schimel, Lynne Hugendubler, Selin Mammen, Dena R. Yver, Samuel W. Cushman, Elisabetta Mueller, Masayuki Yamamoto, Lewis L. Hsu and Constance Tom Noguchi ()
Additional contact information
Ruifeng Teng: Molecular Cell Biology Branch, National Institute of Diabetes and Digestive and Kidney Diseases
Oksana Gavrilova: Mouse Metabolism Core Laboratory
Norio Suzuki: Tohoku University Graduate School of Medicine
Tatyana Chanturiya: Mouse Metabolism Core Laboratory
Daniel Schimel: Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases
Lynne Hugendubler: Mouse Imaging Facility, National Institute of Neurological Disorders and Stroke, National Institutes of Health
Selin Mammen: Molecular Cell Biology Branch, National Institute of Diabetes and Digestive and Kidney Diseases
Dena R. Yver: Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases
Samuel W. Cushman: Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases
Elisabetta Mueller: Mouse Imaging Facility, National Institute of Neurological Disorders and Stroke, National Institutes of Health
Masayuki Yamamoto: Tohoku University Graduate School of Medicine
Lewis L. Hsu: Center for Cancer and Blood Disorders, Children's National Medical Center
Constance Tom Noguchi: Molecular Cell Biology Branch, National Institute of Diabetes and Digestive and Kidney Diseases

Nature Communications, 2011, vol. 2, issue 1, 1-12

Abstract: Abstract Although erythropoietin (Epo) is the cytokine known to regulate erythropoiesis, erythropoietin receptor (EpoR) expression and associated activity beyond haematopoietic tissue remain uncertain. Here we show that mice with EpoR expression restricted to haematopoietic tissues (Tg) develop obesity and insulin resistance. Tg-mice exhibit a decrease in energy expenditure and an increase in white fat mass and adipocyte number. Conversely, Epo treatment of wild-type (WT)-mice increases energy expenditure and reduces food intake and fat mass accumulation but shows no effect in body weight of Tg-mice. EpoR is expressed at a high level in white adipose tissue and in the proopiomelanocortin (POMC) neurons of the hypothalamus. Although Epo treatment in WT-mice induces the expression of the polypeptide hormone precursor, POMC, mice lacking EpoR show reduced levels of POMC in the hypothalamus. This study provides the first evidence that mice lacking EpoR in non-haematopoietic tissue become obese and insulin resistant with loss of Epo regulation of energy homeostasis.

Date: 2011
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DOI: 10.1038/ncomms1526

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