Abstract
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
Highlights
Growth hormone (GH) is a powerful stimulator of lipid oxidation [1] and energy expenditure [2]
The purpose of this study was to investigate whether obese rats with a strong anorectic response to growth hormone 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)
Summary
Growth hormone (GH) is a powerful stimulator of lipid oxidation [1] and energy expenditure [2]. We have previously shown that the excess of body fat of obese rats is broken down within just 3 weeks during pharmacologic exposure to GH and that inhibition of food intake is seen in the first phase of this period [3,4]. In our most recent study, the decrease in food intake was associated with decreased hypothalamic galanin [1]. Further investigations of the physiological events associated with the anorectic effect of GH are principally interesting and motivated. They may provide additional evidence for a link between increased rates of lipid oxidation and inhibition of food intake, and lead to discovery of effective targets for the treatment of obesity. Several authors have suggested that the liver plays a crucial role in this association [5], and that metabolic signals from this organ may affect higher brain centers so that food intake is reduced
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