title: Hypothalamo-pituitary-IGF-1 axis in female rats made obese by overfeeding.
abstract: A gender-related impairment of the somatotrophic axis is present in obese Zucker rats, female rats being better preserved than males. We showed that another animal model of obesity, i.e., male rats made obese by feeding a hypercaloric diet had a reduced function of somatotrophic axis which was likely related to impairment of gonadal function. Aim of this work was that of studying the function of somatotrophic axis in female overfed rats and comparing it to that of male rats of the previous study. Sprague-Dawley female rats were fed an energy-rich palatable diet for seven months. At the end of overfeeding, according to the degree of overweight, rats were divided into overtly obese (Obese), overweight (Overweight) and Non-Obese, i.e. rats whose weights were similar to those of controls. Rats fed ad libitum with the standard pellet chow served as controls (Controls). Acute administration of a supramaximal dose of GHRH (2 microg/rat, iv) elicited a plasma GH rise similar to that of Controls in all the groups, except in Obese which had a lower GH response. Growth hormone responses after GHRH administration were inversely related to plasma levels of free fatty acids (FFA). Pituitary GH content and gene expression as well as hypothalamic GHRH and SS mRNA content, were similar in all experimental groups and in Controls and the same was true for plasma concentrations of free IGF-I. These results indicate that, similarly to obese female Zucker rats, also overfed female rats had a better preservation of the somatotrophic axis than their male counterparts. In diet-induced obese rats, also the etiology of the impairment of somatotrophic axis seems to be gender-related i.e. due to a reduction of gonadal function in males and to an elevation of FFA in females.
authors.affiliation: Dept. Pharmacology, University of Milano.
authors.forename: L
authors.initials: L
authors.lastname: Cattaneo
authors.forename: V
authors.initials: V
authors.lastname: De Gennaro Colonna
authors.forename: M
authors.initials: M
authors.lastname: Zoli
authors.forename: E E
authors.initials: EE
authors.lastname: Müller
authors.forename: D
authors.initials: D
authors.lastname: Cocchi
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D005260:Female; D013006:Growth Hormone / Q000096:biosynthesis / Q000097:blood; D013007:Growth Hormone-Releasing Hormone / Q000494:pharmacology; D006963:Hyperphagia / Q000503:physiopathology*; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D007328:Insulin / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000378:metabolism / Q000502:physiology*; D008297:Male; D009765:Obesity / Q000209:etiology / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012737:Sex Factors
chemical_list: D001786:Blood Glucose; D007328:Insulin; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D013007:Growth Hormone-Releasing Hormone