Glucose homeostasis and insulin sensitivity in growth hormone-transgenic mice: a cross-sectional analysis
In contrast to its stimulatory effects on musculature, bone, and organ development, and its lipolytic effects, growth hormone (GH) opposes insulin effects on glucose metabolism. Chronic GH overexposure is thought to result in insulin insensitivity and decreased blood glucose homeostatic control. Yet...
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Published in | Biological chemistry Vol. 391; no. 10; pp. 1149 - 1155 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Germany
Walter de Gruyter
01.10.2010
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Subjects | |
Online Access | Get full text |
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Summary: | In contrast to its stimulatory effects on musculature, bone, and organ development, and its lipolytic effects, growth hormone (GH) opposes insulin effects on glucose metabolism. Chronic GH overexposure is thought to result in insulin insensitivity and decreased blood glucose homeostatic control. Yet, despite the importance of this concept for basic biology, as well as human conditions of GH excess or deficiency, no systematic assessment of the impact of GH over- expression on glucose homeostasis and insulin sensitivity has been conducted. We report that male and female adult GH transgenic mice have enhanced glucose tolerance compared to littermate controls and this effect is not dependent on age or on the particular heterologous GH transgene used. Furthermore, increased glucose-stimulated insulin secretion, augmented insulin sensitivity, and muted gluconeogenesis were also observed in bovine GH overexpressing mice. These results show that markedly increased systemic GH concentration in GH-transgenic mice exerts unexpected beneficial effects on glucose homeostasis, presumably via a compensatory increase in insulin release. The counterintuitive nature of these results challenges previously held presumptions of the physiology of these mice and other states of GH overexpression or suppression. In addition, they pose intriguing queries about the relationships between GH, endocrine control of metabolism, and aging. |
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Bibliography: | istex:0990487404135CBD94126D539DF203EC2C81FF1A bc.2010.124.pdf ark:/67375/QT4-BRFD5L1K-D ArticleID:bc.2010.124 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 These authors contributed equally to this work. |
ISSN: | 1431-6730 1437-4315 |
DOI: | 10.1515/bc.2010.124 |