Social isolation stress induces hepatic hypertrophy in C57BL/6J mice.

We previously reported that social isolation stimulated a stress response leading to increasing plasma corticosterone level and disruption of the hepatic lipid metabolism-related pathway, without changing body and organ weights, in mice after 4 weeks of social isolation stress, compared with the grouped-housing control (5 mice/cage). In this study, we evaluated the effects of social isolation stress for an extended period on physiologic changes in male C57BL/6J mice. Plasma corticosterone was reduced after 13 weeks, indicating mice might adapt to social isolation stress. However, body and visceral fat weights were significantly increased in combination with hepatic hypertrophy, and significant decreases in levels of triglyceride and adiponectin in plasma were observed. In conclusion, it is tempting to speculate that mice exposed to social isolation stress for 13 continuous weeks could be at an increased risk of overweight with hepatic hypertrophy. Our results also imply that physiological changes, at least fatty acid metabolism, under stress exposure might be an important factor when evaluating the chronic effects of environmental chemicals.

Effects of animal care procedures on plasma corticosterone levels in group-housed mice during the nocturnal active phase.

C57BL/6 mice were housed five per cage on a 12:12 h light/dark cycle. All animal care, including bed cleaning, was carried out during the nonactive phase. After 2 weeks, mean plasma corticosterone levels, collected during the nonactive (ZT6) and active (ZT18) phases, were 66.0 and 270.9 ng/ml, respectively. The values at ZT18 gradually increased in the order of the mice used for blood collection, but not at ZT6. When animal care was carried out at ZT18, the increasing pattern of plasma corticosterone levels previously observed at ZT18 was less pronounced after 2 weeks of acclimatization, and was not observed after 4 weeks. Therefore, animal care should be carried out in the active phase for at least 4 weeks before experiments involving stress responses in the active phase.