title: Social defeat increases food intake, body mass, and adiposity in Syrian hamsters.
abstract: Overeating and increases in body and fat mass are the most common responses to day-to-day stress in humans, whereas stressed laboratory rats and mice respond oppositely. Group housing of Syrian hamsters increases body mass, adiposity, and food intake, perhaps due to social confrontation-induced stress. In experiment 1 we asked, Does repeated social defeat increase food intake, body mass, and white adipose tissue (WAT) mass in Syrian hamsters? Male hamsters subjected to the resident-intruder social interaction model and defeated intermittently 15 times over 34 days for 7-min sessions significantly increased their food intake, body mass, and most WAT masses compared with nondefeated controls. Defeat significantly increased terminal adrenal norepinephrine, but not epinephrine, content. In experiment 2 we asked, Are 15 intermittent resident-intruder interactions necessary to increase body mass and food intake? Body mass and food intake of subordinate hamsters defeated only once were similar to those of nondefeated controls, but four or eight defeats similarly and significantly increased these responses. In experiment 3 we asked, Do intermittent defeats increase adiposity and food intake more than consecutive defeats? Four intermittent or consecutive defeats similarly and significantly increased food intake and body mass compared with nondefeated controls, but only intermittent defeats significantly increased all WAT masses. Consecutive defeats significantly increased mesenteric and inguinal WAT masses. Plasma leptin, but not insulin, concentrations were similarly and significantly increased compared with nondefeated controls. Collectively, social defeat, a natural stressor, significantly increased food intake, body mass, and adiposity in Syrian hamsters and may prove useful in determining mechanisms underlying human stress-induced obesity.
authors.affiliation: Dept. of Biology, Georgia State Univ., 24 Peachtree Center Ave. NE, Atlanta, GA 30302-4010, USA.
authors.forename: Michelle T
authors.initials: MT
authors.lastname: Foster
authors.forename: Matia B
authors.initials: MB
authors.lastname: Solomon
authors.forename: Kim L
authors.initials: KL
authors.lastname: Huhman
authors.forename: Timothy J
authors.initials: TJ
authors.lastname: Bartness
mesh_terms: D000273:Adipose Tissue / Q000502:physiology*; D000311:Adrenal Glands / Q000033:anatomy & histology / Q000254:growth & development / Q000378:metabolism; D000818:Animals; D001835:Body Weight / Q000502:physiology*; D002395:Catecholamines / Q000378:metabolism; D006224:Cricetinae; D004435:Eating / Q000502:physiology*; D006854:Hydrocortisone / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D008647:Mesocricetus; D009929:Organ Size / Q000502:physiology; D011863:Radioimmunoassay; D012930:Social Dominance; D013154:Spleen / Q000033:anatomy & histology / Q000502:physiology; D013737:Testis / Q000033:anatomy & histology / Q000502:physiology; D013950:Thymus Gland / Q000033:anatomy & histology / Q000502:physiology
chemical_list: D002395:Catecholamines; D020738:Leptin; D006854:Hydrocortisone