title: Differential effects of glucocorticoids on energy homeostasis in Syrian hamsters.
abstract: Syrian hamsters, like many humans, increase food intake and body adiposity in response to stress. We hypothesized that glucocorticoids (cortisol and corticosterone) mediate these stress-induced effects on energy homeostasis. Because Syrian hamsters are dual secretors of cortisol and corticosterone, differential effects of each glucocorticoid on energy homeostasis were investigated. First, adrenal intact hamsters were injected with varying physiological concentrations of cortisol, corticosterone, or vehicle to emulate our previously published defeat regimens (i.e., 1 injection/day for 5 days). Neither food intake nor body weight was altered following glucocorticoid injections. Therefore, we investigated the effect of sustained glucocorticoid exposure on energy homeostasis. This was accomplished by implanting hamsters with supraphysiological steady-state pellets of cortisol, corticosterone, or cholesterol as a control. Cortisol, but not corticosterone, significantly decreased food intake, body mass, and lean and fat tissue compared with controls. Despite decreases in body mass and adiposity, cortisol significantly increased circulating free fatty acids, triglyceride, cholesterol, and hepatic triglyceride concentrations. Although corticosterone did not induce alterations in any of the aforementioned metabolic end points, Syrian hamsters were responsive to the effects of corticosterone since glucocorticoids both induced thymic involution and decreased adrenal mass. These findings indicate that cortisol is the more potent glucocorticoid in energy homeostasis in Syrian hamsters. However, the data suggest that cortisol alone does not mediate stress-induced increases in food intake or body mass in this species.
authors.affiliation: Department of Psychiatry and Behavioral Neuroscience, Obesity Research Center, Metabolic Disease Institute, University of Cincinnati, 2170 E. Galbraith Rd., Cincinnati, OH 45237, USA.
authors.forename: Matia B
authors.initials: MB
authors.lastname: Solomon
authors.forename: Randall R
authors.initials: RR
authors.lastname: Sakai
authors.forename: Stephen C
authors.initials: SC
authors.lastname: Woods
authors.forename: Michelle T
authors.initials: MT
authors.lastname: Foster
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D002784:Cholesterol / Q000097:blood; D003345:Corticosterone / Q000378:metabolism* / Q000494:pharmacology; D006224:Cricetinae; D003480:Cushing Syndrome / Q000139:chemically induced / Q000378:metabolism*; D004435:Eating / Q000187:drug effects / Q000502:physiology; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology*; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology*; D006854:Hydrocortisone / Q000378:metabolism* / Q000494:pharmacology; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000502:physiology; D007328:Insulin / Q000097:blood; D050356:Lipid Metabolism / Q000187:drug effects / Q000502:physiology; D008297:Male; D008647:Mesocricetus / Q000378:metabolism*; D009765:Obesity / Q000378:metabolism; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000502:physiology; D013045:Species Specificity; D013312:Stress, Physiological / Q000502:physiology; D014280:Triglycerides / Q000097:blood
chemical_list: D007328:Insulin; D014280:Triglycerides; D002784:Cholesterol; D003345:Corticosterone; D006854:Hydrocortisone