title: Intracerebroventricular infusion of leptin elevates the secretion of luteinising hormone without affecting food intake in long-term food-restricted sheep, but increases growth hormone irrespective of bodyweight.
abstract: Leptin can act as a satiety factor and exert neuroendocrine effects, but most studies have been performed in fasted animals. We aimed to determine the effect of chronic under-nutrition on the response to a 3-day intracerebroventricular infusion of leptin with regard to food intake and the secretion of pituitary hormones. Ovariectomised ewes (n=6) had a mean (+/-s.e.m. ) bodyweight of 56+/-0.8 kg on a diet available ad libitum (ad lib) or 33.4+/-1 kg on a restricted diet. The differential bodyweight was achieved by dietary means over a period of 6 months prior to the commencement of the study. Leptin (4 microg/h) or vehicle (artificial cerebrospinal fluid (aCSF)) was infused into the third cerebral ventricle for 3 days. Blood samples were taken prior to commencement and on day 3 of infusion for the assay of plasma hormone levels. The experiment was repeated one week later in a cross-over design. Food intake and metabolic status were monitored daily. The luteinising hormone (LH) pulse amplitude was lower (P<0.05) but plasma growth hormone (GH) levels were higher (P<0.05) in the food-restricted animals. Plasma levels of glucose, lactate, insulin, urea and triglycerides were similar in the two groups but non-esterified fatty acid levels were higher (P<0.01) in the animals on an ad lib diet. Leptin reduced (P<0.05) food intake only in the animals fed an ad lib diet. Leptin increased (P<0.05) the secretion of LH in the food-restricted group only and increased (P<0.05) GH irrespective of bodyweight. In conclusion, leptin does not alter food intake in animals on a restricted diet but can increase the secretion of LH in the same animals. The treatment of leptin was not sufficient to reduce plasma GH levels in the food-restricted animals, suggesting that other factors or mechanisms must be involved in the regulation of this axis.
authors.affiliation: Prince Henry's Institute of Medical Research, PO Box 5152 Clayton, Victoria 3168, Australia.
authors.forename: B A
authors.initials: BA
authors.lastname: Henry
authors.forename: J W
authors.initials: JW
authors.lastname: Goding
authors.forename: A J
authors.initials: AJ
authors.lastname: Tilbrook
authors.forename: F R
authors.initials: FR
authors.lastname: Dunshea
authors.forename: I J
authors.initials: IJ
authors.lastname: Clarke
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D002908:Chronic Disease; D018592:Cross-Over Studies; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood / Q000378:metabolism; D013006:Growth Hormone / Q000097:blood / Q000378:metabolism*; D007276:Injections, Intraventricular; D020738:Leptin / Q000008:administration & dosage* / Q000494:pharmacology; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism*; D009748:Nutrition Disorders / Q000503:physiopathology*; D010052:Ovariectomy; D012528:Satiety Response / Q000187:drug effects*; D012756:Sheep
chemical_list: D005230:Fatty Acids, Nonesterified; D020738:Leptin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013006:Growth Hormone