Chronic erythropoietin treatment improves diet-induced glucose intolerance in rats
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Chronic erythropoietin treatment improves diet-induced glucose intolerance in rats. / Caillaud, Corinne; Mechta, Mie; Ainge, Heidi; Madsen, Andreas Nygaard; Ruell, Patricia; Mas, Emilie; Bisbal, Catherine; Mercier, Jacques; Twigg, Stephen; Mori, Trevor A; Simar, David; Barrès, Romain.
In: Journal of Endocrinology, Vol. 225, No. 2, 2015, p. 77-88.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Chronic erythropoietin treatment improves diet-induced glucose intolerance in rats
AU - Caillaud, Corinne
AU - Mechta, Mie
AU - Ainge, Heidi
AU - Madsen, Andreas Nygaard
AU - Ruell, Patricia
AU - Mas, Emilie
AU - Bisbal, Catherine
AU - Mercier, Jacques
AU - Twigg, Stephen
AU - Mori, Trevor A
AU - Simar, David
AU - Barrès, Romain
N1 - © 2015 The authors.
PY - 2015
Y1 - 2015
N2 - Erythropoietin (EPO) ameliorates glucose metabolism through mechanisms not fully understood. In this study, we investigated the effect of EPO on glucose metabolism and insulin signaling in skeletal muscle. A 2-week EPO treatment of rats fed with a high-fat diet (HFD) improved fasting glucose levels and glucose tolerance, without altering total body weight or retroperitoneal fat mass. Concomitantly, EPO partially rescued insulin-stimulated AKT activation, reduced markers of oxidative stress, and restored heat-shock protein 72 expression in soleus muscles from HFD-fed rats. Incubation of skeletal muscle cell cultures with EPO failed to induce AKT phosphorylation and had no effect on glucose uptake or glycogen synthesis. We found that the EPO receptor gene was expressed in myotubes, but was undetectable in soleus. Together, our results indicate that EPO treatment improves glucose tolerance but does not directly activate the phosphorylation of AKT in muscle cells. We propose that the reduced systemic inflammation or oxidative stress that we observed after treatment with EPO could contribute to the improvement of whole-body glucose metabolism.
AB - Erythropoietin (EPO) ameliorates glucose metabolism through mechanisms not fully understood. In this study, we investigated the effect of EPO on glucose metabolism and insulin signaling in skeletal muscle. A 2-week EPO treatment of rats fed with a high-fat diet (HFD) improved fasting glucose levels and glucose tolerance, without altering total body weight or retroperitoneal fat mass. Concomitantly, EPO partially rescued insulin-stimulated AKT activation, reduced markers of oxidative stress, and restored heat-shock protein 72 expression in soleus muscles from HFD-fed rats. Incubation of skeletal muscle cell cultures with EPO failed to induce AKT phosphorylation and had no effect on glucose uptake or glycogen synthesis. We found that the EPO receptor gene was expressed in myotubes, but was undetectable in soleus. Together, our results indicate that EPO treatment improves glucose tolerance but does not directly activate the phosphorylation of AKT in muscle cells. We propose that the reduced systemic inflammation or oxidative stress that we observed after treatment with EPO could contribute to the improvement of whole-body glucose metabolism.
U2 - 10.1530/JOE-15-0010
DO - 10.1530/JOE-15-0010
M3 - Journal article
C2 - 25767056
VL - 225
SP - 77
EP - 88
JO - Journal of Endocrinology
JF - Journal of Endocrinology
SN - 0022-0795
IS - 2
ER -
ID: 138136881