The relationship between major depressive disorder and glucose parameters: A cross-sectional study in a Chinese population.

Abstract

Depressive symptoms have been linked with insulin resistance in middle-aged and elderly populations. A strong relationship between peripheral insulin resistance and glucose homeostasis imbalance has been well established in previous studies. The role of serum fructosamine and fasting blood glucose (FBG) in elevating glucose homeostasis has been documented in the literature. The aim of the study was to examine the association of serum fructosamine and FBG with major depressive disorder (MDD). The study analyzed the clinical characteristics and biochemical parameters of 305 patients with MDD and 312 healthy individuals. Serum concentrations of lipoprotein-cholesterol (HDL-C), total protein (TP) and creatinine (Cr) were found to be significantly different between the two groups. Serum fructosamine and fasting blood glucose (FBG) concentrations were high in patients with MDD compared with healthy individuals (2.3 ± 0.26 vs. 2.1 ± 0.27, p = 0.018; 4.7 ± 0.45 vs. 4.5 ± 0.45, p < 0.001). The levels of serum fructosamine and FBG were also significantly higher in patients with MDD when all participants were stratified by gender. Age was found to be positively correlated with FBG, serum fructosamine and Cr (r = 0.203, p < 0.001; r = 0.129, p = 0.025; r = 0.129, p = 0.024), and negatively correlated with TP (r = -0.114, p = 0.047) in patients with MDD. However, there were no correlations between age and FBG, serum fructosamine or Cr in the healthy controls. In a multivariate logistic regression analysis, increased serum fructosamine and FBG concentrations were positively associated with MDD independently of age and gender, after adjustment for age and potential confounding factors (OR = 6.313, CI95 %:2.953-13.393, p < 0.001; OR = 2.251, CI95 %: 1.464-3.462, p < 0.001). The study results suggest that increased serum fructosamine and FBG concentrations are associated with depressive conditions, which may influence glucose metabolism and impair glucose homeostasis in patients with MDD.