Objective Reports regarding the associations between childhood maltreatment (CM) and body fat composition remain heterogeneous in humans although it is indicated in preclinical studies. Moreover, the effects of CM subtypes on different types of body fat are unclear. Thus this study is to determine the associations between CM and its subtypes with body fat and to explore the potential pathways. Methods Participants were assessed for a history of CM by the Childhood Trauma Questionnaire, and were divided into the CM group (with CM exposures) and non-CM group (without CM exposures). Body composition was measured by dual-energy X-ray absorptiometry. Subjects provided salivary and blood samples. Results Compared with the non-CM group, CM subjects had greater visceral fat mass (1136±160g vs. 836±116g, p<0.05) but not total body fat, android fat, body mass index or waist-to-hip ratio. Moreover, CM subjects had a blunted cortisol awakening response and elevated inflammatory factors. Correlation analysis indicated that CM subtypes had differential effects on visceral adiposity and cortisol awakening response. Conclusions Our results suggest that CM exposure is linked with increased visceral fat deposition, and the perturbation of the HPA axis activity and activation of the immune system may be 2 potential pathways that explain this relationship.

Reports regarding the associations between major depressive disorder (MDD) and diabetes remain heterogeneous. Our aim was to investigate whether glucose homeostasis and insulin sensitivity were impaired in the MDD patients and its mechanisms. A total of 30 patients with MDD and 30 matched controls were recruited. The oral glucose tolerance test and dual-energy X-ray absorptiometry scan were performed in each participant. Insulin signaling in postmortem brain tissues from other depressive patients and controls (obtained from Alabama brain bank) was examined. Insulin sensitivity was reduced substantially in the MDD patients, however, the fasting and 2-h glucose concentrations remained within the normal range through compensatory insulin secretion. Despite increased insulin secretion, 1-h glucose concentrations in the MDD patients were significantly elevated compared with the controls. MDD patients had greater visceral fat mass but lower adiponectin levels compared with the controls. Furthermore, phosphorylated-AKT levels in insulin signaling were decreased in postmortem brain tissues in patients with MDD. These results suggest that MDD patients are at a greater risk for diabetes due to decreased insulin sensitivity, reduced disposition index, and impaired glucose tolerance as manifested by elevated 1-h glucose concentrations following an oral glucose challenge. Mechanistic studies reveal that decreased insulin sensitivity is associated with increased visceral fat mass, lower adiponectin levels and impaired insulin action in postmortem brain tissues in the MDD patients. Our findings emphasize the importance of screening depressive patients to identify susceptible individuals for developing future diabetes with the hope of improving their health outcomes.

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