Evaluation of the relationship between glucagon-like peptide 1 (GLP-1) level, TNF-α level and metabolic parameters with symptom severity in newly diagnosed major depressive disorder patients after six months of treatment

INTRODUCTION AND AIM: In our study, we aimed to compare the levels of TNF-α and GLP-1 in patients with major depressive disorder at the time of initial diagnosis and after 6 months of treatment, to investigate whether these markers changed after 6 months of treatment compared to the pre-treatment period, and to investigate whether the change in these parameters was associated with the change in the severity of depression in patients, and to contribute to the development of new biomarkers that can be used to elucidate the etiology of depression and to evaluate the response to treatment. METHODS AND TOOLS: This study was conducted with 40 patients, when they admitted to the Psychiatry Outpatient Clinic of Balıkesir University Health Practice and Research Hospital, who were administered SCID-5-CV and diagnosed with major depressive disorder for the first time according to DSM-V diagnostic criteria and started to receive psychiatric treatment for the first time and continued psychiatric treatment for six months. Sociodemographic data form was given to the patients after the consent form at the time of admission, Hamilton Depression Rating Scale and Hamilton Anxiety Rating Scale were administered, serum GLP-1 and TNF-α levels were measured and fasting blood glucose, HbA1c, HDL, LDL, total cholesterol, triglyceride, waist circumference and arterial blood pressure values were measured to evaluate metabolic parameters before the initiation of treatment and in the sixth month of treatment. The 6-month changes in these values were analyzed by statistical methods. RESULTS: GLP-1 values of the patients decreased from 69.2 ± 58.1 pmol/L before treatment to 60.1 ± 50.6 pmol/L after treatment, but the difference was not significant (p = 0.085). In addition, TNF-α value decreased significantly from 357.0 ± 343.0 ng/L before treatment to 238.2 ± 221.6 ng/L after treatment (p = 0.005). The mean Hamilton Depression Rating Scale (HAM-D) scores of the patients decreased significantly from 19.3 ± 4.5 before treatment to 14.3 ± 6.4 after treatment (t = 5.498, p < 0.001). In addition, the mean Hamilton Anxiety Rating Scale (HAM-A) scores decreased significantly from 10.7 ± 2.5 before treatment to 6.7 ± 3.9 after treatment (t = 7.094, p < 0.001). Correlation analysis was performed to examine the relationship between changes in HAM-D, HAM-A scores and changes in GLP-1 and TNF-α levels. A significant positive correlation was found between the change in the mean GLP-1 level and changes in both mean HAM-D and HAM-A scores (p=0.041, r=0.324; p=0.035, r=0.334). Moreover, a significant positive correlation was observed between the change in mean TNF-α level and changes in both mean HAM-D and HAM-A scores (p=0.014, r=0.385; p=0.025, r=0.355). A significant positive correlation was also found between the change in mean HAM-D score and the change in mean HAM-A score (p=0.001, r=0.521). Furthermore, a significant positive correlation was found between the change in mean TNF-α level and the change in mean GLP-1 level (p=0.000, r=0.917). CONCLUSION: Our study revealed that GLP-1 and TNF-α levels may be associated with symptom severity in patients with major depressive disorder. However, since this relationship between depression and GLP-1 and TNF-α may be bidirectional, it can be said that both markers may play a role in the pathophysiology of major depressive disorder. It is not yet known whether the occurrence and aggravation of depressive symptoms leads to an increase in GLP-1 and TNF- α levels or whether an increase in GLP-1 and TNF- α levels causes depressive symptoms. Although the findings in our study provide important contributions to our understanding of the pathophysiology of major depressive disorder, further studies with a larger sample, focusing on determining the direction of this relationship and revealing the causal link are needed.