Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-27217
Katz, O; Stuible, M; Golishevski, N; Lifshitz, L; Tremblay, M; Gassmann, M; Mittelman, M; Neumann, D (2010). Erythropoietin treatment leads to reduced blood glucose levels and body mass: Insights from murine models. Journal of Endocrinology, 205(1):87-95.
Erythropoietin (EPO) regulates proliferation and differentiation of erythroid precursor cells into erythrocytes. The last decade has revealed non-renal sites of EPO production and extrahematopoietic expression of the EPO-receptor (EPO-R), thus suggesting that EPO has pleiotropic functions. Here we addressed the interplay between EPO / glucose metabolism / body weight, by employing a panel of relevant experimental murine models. The models focused on situations of increased EPO levels, including EPO injected C57BL/6 and BALB/c mice, as well as transgenic mice (tg6) constitutively overexpressing human EPO, thus exposed to constantly high EPO serum levels. As experimental models for diabetes and obesity, we employed protein Tyr phosphatase 1B (PTP1B) knockout mice associated with resistance to diabetes (PTP1B-/-), and ob/ob mice susceptible to diabetes and obesity. The data presented herein demonstrate EPO-mediated decrease in blood glucose levels in all mice models tested. Moreover, in the ob/ob mice we observed EPO-mediated attenuation of body weight gain and reduction of hemoglobin A1C. Taken together our data bear significant clinical implications of EPO treatment in the management of a wide range of metabolic diseases, thus adding an important novel therapeutic potential to this pleiotropic hormone.
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||05 Vetsuisse Faculty > Institute of Veterinary Physiology|
04 Faculty of Medicine > Center for Integrative Human Physiology
|DDC:||570 Life sciences; biology|
610 Medicine & health
|Deposited On:||22 Jan 2010 06:16|
|Last Modified:||28 Nov 2013 01:39|
|Publisher:||Society for Endocrinology|
|Additional Information:||Disclaimer. This is not the definitive version of record of this article. This manuscript has been accepted for publication in Journal of Endocrinology, but the version presented here has not yet been copy edited, formatted or proofed. Consequently, the Society for Endocrinology accepts no responsibility for any errors or omissions it may contain. The definitive version is now freely available at 10.1677/JOE-09-0425. © 2010 Society for Endocrinology|
|Free access at:||Publisher DOI. An embargo period may apply.|
|Citations:||Web of Science®. Times cited: 10|
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