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The anorectic response to growth hormone in obese rats is associated with increased ketogenesis: A short communication

Author(s): Bo Xu | Manjunath Manubolu | Paresh Dutta | Kjell Malmlöf

Journal: Open Journal of Molecular and Integrative Physiology
ISSN 2162-2159

Volume: 03;
Issue: 02;
Start page: 80;
Date: 2013;
Original page

Keywords: Growth Hormone | Lipolysis | Ketogenesis | Food Intake

The purpose of this study was to investigate whether obese rats with a strong anorectic response to growth hormone also showed signs of increased hepatic ketogenesis as reflected in circulating β-hydroxybutyrate levels. Rats with diet-induced obesity were allocated to one of two groups, receiving either vehicle (n = 7) or 4 mg/kg/d of growth hormone (n = 13) for 4 days. This latter group was later split into a group of responders (n = 8) showing a cumulated reduction of food intake of more than 4 g from base line during the last two days of administrations and a group of non-responders (n = 5). The cumulated reduction of food intake from baseline among the responders was 10.8 ±1.5 g. The corresponding marginal reductions in the non-responder and vehicle groups were 0.5 ±3.4 gand 0.5 ±3.7 g, respectively. Growth hormone administration generally increased serum levels of β-hydroxybutyrate and free fatty acids, compared with vehicle, whereas triglycerides were decreased. Among the responders this effect was statistically significant in all instances whereas the same trend was weaker among non-responders. The main finding of the present study was that the serum β-hydroxybutyrate levels of 0.76 ± 0.11 mmol/l among responders was three times higher than non-responders (p < 0.01). In conclusion, the present study suggests that increased hepatic ketogenesis is an important component in the mechanism by which growth hormone inhibits food intake in rats with an obese phenotype. The precise molecular mechanisms, however, remain to be elucidated.
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