title: The anorectic response to growth hormone in obese rats is associated with an increased rate of lipid oxidation and decreased hypothalamic galanin.
abstract: The aim of this study was to demonstrate differential effects of growth hormone (GH) on food intake in lean and obese rats and to investigate whether an anticipated anorectic response in obese rats might be associated with increased lipid oxidation and altered hypothalamic neuropeptide levels. GH (4 mg/kg/day) was administered during 5-21 days to non-obese and obese rats. Whereas GH stimulated food intake in the non-obese rats, the obese animals responded with a significantly (p<0.05) suppressed food intake for 4-5 days. On day 4, the obese rats injected with GH and those injected with vehicle consumed 9.2 ± 0.66 g and 12.7 ± 1.05 g, respectively. The suppression of food intake was associated with significantly (p<0.05) increased lipid oxidation. A similar, but statistically not verified, trend was seen in pair-fed rats not exposed to GH. However, while these animals appeared to economize their energy expenditure, the GH-exposed animals did not, thus creating a significant (p<0.05) difference between these two groups. The increased lipid oxidation and energy expenditure observed in the rats exposed to GH were associated with significantly (p<0.05) decreased levels of hypothalamic galanin (111 ± 33.2 pmol/g vs. those of the pair-fed controls: 228.5 ± 49.4 pmol/g). This difference was, however, not sustained. Thus, on day 21 both hypothalamic galanin and the food intake in the GH group were back to normal. Hypothalamic NPY remained unchanged by GH at all times. In conclusion, the present study suggests that increased lipid oxidation and decreased hypothalamic galanin are components in the mechanism by which GH inhibits food intake in an obese phenotype.
authors.affiliation: Department of Anatomy, Physiology and Biochemistry, Faculty of Veterinary Medicine and Animal Science, SLU, Uppsala, Sweden. Kjell.Malmlof@afb.slu.se
authors.forename: Kjell
authors.initials: K
authors.lastname: Malmlöf
authors.forename: Christian
authors.initials: C
authors.lastname: Fledelius
authors.forename: Thue
authors.initials: T
authors.lastname: Johansen
authors.forename: Elvar
authors.initials: E
authors.lastname: Theodorsson
mesh_terms: D000818:Animals; D018752:Diet, Fat-Restricted; D004041:Dietary Fats / Q000494:pharmacology; D004435:Eating / Q000187:drug effects*; D004734:Energy Metabolism / Q000187:drug effects; D005260:Female; D019004:Galanin / Q000378:metabolism*; D013006:Growth Hormone / Q000494:pharmacology / Q000502:physiology*; D007031:Hypothalamus / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D020738:Leptin / Q000097:blood; D050356:Lipid Metabolism / Q000187:drug effects*; D008055:Lipids / Q000097:blood; D009478:Neuropeptide Y / Q000378:metabolism; D009765:Obesity / Q000097:blood / Q000378:metabolism*; D010084:Oxidation-Reduction / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D013963:Thyroid Hormones / Q000097:blood
chemical_list: D004041:Dietary Fats; D007328:Insulin; D020738:Leptin; D008055:Lipids; D009478:Neuropeptide Y; D013963:Thyroid Hormones; D007334:Insulin-Like Growth Factor I; D019004:Galanin; D013006:Growth Hormone