Abstract | UNLABELLED: The aim of this study was to determine the effects of intermittent hypoxia training (IHT), with and without fatty-diet, on bodyweight, serum glucose, leptin, insulin, and their receptors, and to test whether erythropoietin (EPO) mediates these effects. METHODS: Kunming mice were divided into four groups. 1: untreated control; 2: IHT; 3: fatty-diet; 4: fatty-diet and IHT. After 40 days exposure to IHT, the bodyweight, serum glucose, serum leptin, insulin and EPO were measured by ELISA. Liver leptin and insulin receptors were quantified. A separate set of mice were treated with several doses of EPO (0-320 U/kg i.p.) for 5 days. In addition, human hepatic cell lines were treated with EPO for 24h and the expression of genes OB-Ra, OB-Rb and IR were measured using RT-PCR. RESULTS: IHT reduced bodyweight and serum glucose, with corresponding increases in the serum levels of leptin, insulin, EPO and expression of leptin and insulin receptors in liver. Repeated EPO treatment increased serum leptin concentration, but had no effects on insulin levels. The expression of the genes OB-Ra, OB-Rb and IR were increased after EPO treatment. CONCLUSION: We postulate that, in mice, IHT reduces bodyweight and serum glucose by increasing EPO synthesis which secondarily increases leptin and insulin production in liver.
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Authors | Ling Qin, Yang Xiang, Zhi Song, Ran Jing, Chengping Hu, Susan T Howard |
Journal | Regulatory peptides
(Regul Pept)
Vol. 165
Issue 2-3
Pg. 168-73
(Dec 10 2010)
ISSN: 1873-1686 [Electronic] Netherlands |
PMID | 20655957
(Publication Type: Journal Article, Retracted Publication)
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Copyright | Copyright © 2010 Elsevier B.V. All rights reserved. |
Chemical References |
- Blood Glucose
- Leptin
- Recombinant Proteins
- Erythropoietin
- Receptor, Insulin
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Topics |
- Animals
- Blood Glucose
(metabolism)
- Body Weight
(physiology)
- Cell Line
- Enzyme-Linked Immunosorbent Assay
- Erythropoietin
(blood, metabolism, pharmacology)
- Female
- Humans
- Hypoxia
(blood, physiopathology)
- Leptin
(blood)
- Liver
(drug effects, metabolism)
- Mice
- Receptor, Insulin
(genetics)
- Recombinant Proteins
- Reverse Transcriptase Polymerase Chain Reaction
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