Metabolic consequences and vulnerability to diet-induced obesity in male mice under chronic social stress.
Social and psychological factors interact with genetic predisposition and dietary habit in determining obesity. However, relatively few pre-clinical studies address the role of psychosocial factors in metabolic disorders. Previous studies from our laboratory demonstrated in male mice: 1) opposite status-dependent effect on body weight gain under chronic psychosocial stress; 2) a reduction in body weight in individually housed (Ind) male mice. In the present study these observations were extended to provide a comprehensive characterization of the metabolic consequences of chronic psychosocial stress and individual housing in adult CD-1 male mice. Results confirmed that in mice fed standard diet, dominant (Dom) and Ind had a negative energy balance while subordinate (Sub) had a positive energy balance. Locomotor activity was depressed in Sub and enhanced in Dom. Hyperphagia emerged for Dom and Sub and hypophagia for Ind. Dom also showed a consistent decrease of visceral fat pads weight as well as increased norepinephrine concentration and smaller adipocytes diameter in the perigonadal fat pad. On the contrary, under high fat diet Sub and, surprisingly, Ind showed higher while Dom showed lower vulnerability to obesity associated with hyperphagia. In conclusion, we demonstrated that social status under chronic stress and individual housing deeply affect mice metabolic functions in different, sometime opposite, directions. Food intake, the hedonic response to palatable food as well as the locomotor activity and the sympathetic activation within the adipose fat pads all represent causal factors explaining the different metabolic alterations observed. Overall this study demonstrates that pre-clinical animal models offer a suitable tool for the investigation of the metabolic consequences of chronic stress exposure and associated psychopathologies.
Bartolomucci
Alessandro
A
Department of Evolutionary and Functional Biology, University of Parma, Parma, Italy. alessandro.bartolomucci@unipr.it
Cabassi
Aderville
A
Govoni
Paolo
P
Ceresini
Graziano
G
Cero
Cheryl
C
Berra
Daniela
D
Dadomo
Harold
H
Franceschini
Paolo
P
Dell'Omo
Giacomo
G
Parmigiani
Stefano
S
Palanza
Paola
P
D000273:Adipose Tissue / Q000503:physiopathology; D000374:Aggression; D000818:Animals; D001835:Body Weight / Q000502:physiology; D003345:Corticosterone / Q000097:blood; D004032:Diet / Q000009:adverse effects; D004041:Dietary Fats / Q000008:administration & dosage; D004195:Disease Models, Animal; D004291:Dominance-Subordination; D006799:Housing, Animal; D006963:Hyperphagia / Q000523:psychology; D008297:Male; D008659:Metabolic Diseases / Q000209:etiology* / Q000523:psychology; D051379:Mice; D009043:Motor Activity; D009638:Norepinephrine / Q000097:blood; D009765:Obesity / Q000209:etiology* / Q000523:psychology; D012931:Social Environment; D012934:Social Isolation / Q000523:psychology; D013315:Stress, Psychological / Q000150:complications* / Q000523:psychology; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D015430:Weight Gain / Q000502:physiology
D004041:Dietary Fats; D014446:Tyrosine 3-Monooxygenase; D003345:Corticosterone; D009638:Norepinephrine