title: Adrenalectomy and castration in the genetically obese (ob/ob) mouse.
abstract: The present studies have tested the hypothesis that adrenalectomy could modify the phenotypic expression of genetic obesity by examining the effects of adrenalectomy on the function of the gonadal system in lean and ob/ob mice. Corticosterone concentrations were undetectable in the adrenalectomized animals. Adrenalectomy significantly slowed the weight gain of obese mice in comparison to sham-adrenalectomized controls. Gonadectomy had no independent effect on weight gain. The testes, prostate, and seminal vesicles in the ob/ob mice were significantly smaller than in the lean animals. Castration lowered the weights of the prostate and seminal vesicles in the lean mice to weights close to those observed in the castrated ob/ob mice. Castration significantly increased the concentrations of LH and FSH in both ob/ob and lean mice, but the absolute concentrations were higher in the lean mice in both conditions. Adrenalectomy per se had no effect on the concentration of LH, FSH, or testosterone or on the weights of the prostate or seminal vesicles. These data indicate that adrenalectomy has no effect on the physiologic control of the reproductive system in genetically obese mice, and are consistent with the hypothesis that the defect in the ob/ob mouse is a modulator of steroid action which over expresses glucocorticoid effects and under expresses gonadal steroid effects.
authors.affiliation: Section of Diabetes and Clinical Nutrition, University of Southern California, School of Medicine, Los Angeles, CA 90033, USA.
authors.forename: H
authors.initials: H
authors.lastname: Shimizu
authors.forename: K
authors.initials: K
authors.lastname: Ohshima
authors.forename: G A
authors.initials: GA
authors.lastname: Bray
authors.forename: M
authors.initials: M
authors.lastname: Peterson
authors.forename: R S
authors.initials: RS
authors.lastname: Swerdloff
mesh_terms: D000311:Adrenal Glands / Q000378:metabolism / Q000473:pathology*; D000315:Adrenalectomy; D000818:Animals; D001835:Body Weight; D002369:Castration; D003345:Corticosterone / Q000494:pharmacology; D005260:Female; D005640:Follicle Stimulating Hormone / Q000378:metabolism; D005938:Glucocorticoids / Q000378:metabolism; D007986:Luteinizing Hormone / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008820:Mice, Obese; D008822:Mice, Transgenic; D009765:Obesity / Q000473:pathology; D009929:Organ Size; D010641:Phenotype; D011467:Prostate / Q000473:pathology; D012669:Seminal Vesicles / Q000473:pathology; D013256:Steroids / Q000378:metabolism; D013737:Testis / Q000378:metabolism / Q000473:pathology; D013739:Testosterone / Q000378:metabolism; D013997:Time Factors
chemical_list: D005938:Glucocorticoids; D013256:Steroids; D013739:Testosterone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D003345:Corticosterone