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Erythropoietin treatment leads to reduced blood glucose levels and body mass: Insights from murine models


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.

Abstract

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.

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.

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Additional indexing

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
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2010
Deposited On:22 Jan 2010 05:16
Last Modified:05 Apr 2016 13:44
Publisher:Society for Endocrinology
ISSN:0022-0795
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.
Publisher DOI:https://doi.org/10.1677/JOE-09-0425
PubMed ID:20061512
Permanent URL: https://doi.org/10.5167/uzh-27217

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