Abstract

Growing evidence suggests that mood disorder is associated with insulin resistance and inflammation. Thus the effects of antidepressants on insulin sensitivity and proinflammatory responses will be a crucial issue for depression treatment. In this study, we enrolled 43 non-diabetic young depressed males and adapted standard testing procedures to assess glucose metabolism during 4-week hospitalization. Before and after the 4-week antidepressant treatment, participants underwent oral glucose tolerance test (OGTT) and frequently sampled intravenous glucose tolerance test (FSIGT). Insulin sensitivity (SI), glucose effectiveness (SG), acute insulin response, and disposition index (DI) were estimated using the minimal model method. The plasma levels of C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and adiponectin were measured. The Hamilton depression rating scale (HAM-D) total scores were reduced significantly during the course of treatment. There were no significant changes in the parameters of SI, SG, and DI. Compared to drug naïve status, the level of plasma IL-6 was significantly elevated (0.77 to 1.30 pg/ml; P = .001) after antidepressant therapy. However, the concentrations of CRP, TNF-α, and adiponectin showed no differences during the course of treatment. The results suggest that antidepressants may promote stimulatory effect on the IL-6 production in the early stage of antidepressant treatment.

Highlights

  • Depressive disorder is a complex and multifactorial disorder with biological heterogeneity

  • Some studies have demonstrated that depressed individuals had higher glucose levels and insulin resistance when they are symptomatic [3,4,5,6]

  • The randomized treatment groups were similar for age, body weight, body mass index (BMI) and Hamilton depression rating scale (HAM-D) scores

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Summary

Introduction

Depressive disorder is a complex and multifactorial disorder with biological heterogeneity. Growing evidence suggests the mood disorder is associated with insulin resistance and inflammation [1, 2]. Findings suggest an overlapping pathophysiology between depressive disorder and insulin regulation. Some studies have demonstrated that depressed individuals had higher glucose levels and insulin resistance when they are symptomatic [3,4,5,6]. Epidemiologic evidences showed that obesity correlated with depression, and depressed adults have a 37% increased risk of developing type 2 diabetes [7,8,9]. Population-based surveys have evidenced that the prevalence rate of depression in diabetes is around 8% to 25% and up to

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