Abstract
Depression is a comorbid condition in patients with Type 2 Diabetes mellitus (T2DM). S100B, a glia derived protein, is linked to depression and has been suggested as a biomarker for depression outcomes in several populations. However, to date there is no data about S100B levels and depression in patients with T2DM. Objective. We hypothesized that S100B serum levels are increased in patients with T2DM and recently diagnosed, drug-free depressive symptoms, and could be used for the diagnosis of depression in T2DM. Methods. Overall 52 patients (62 ± 12 years, female 66, 7%) with no history of depression deriving from the Diabetes out-patient clinic of our University Hospital underwent a one-to-one interview with a psychiatrist and filled a self-assessment (Zung) questionnaire. Serum S00B levels were compared between 30 (63±12 years, female 66, 7%) diabetic patients without depressive symptoms vs 22 patients (62 ±12 years, female 68, 2%) with T2DM and depressive symptoms. Results. There was no difference in serum levels of S100B between patients with T2DM without depressive symptoms vs diabetic patients suffering from depressive symptoms (2.1 (1.9-10.9) pg/ml vs 2.4 (1.9-14.8) pg/ml, p=0. 637+). Moreover, linear regression analysis did not show any association between lnS100B levels and depressive symptoms (β = 0.084, 95% CI 0.470-0.871, and p=0.552), Zung self-assessment score (β = 0.048, 95% CI -0.024-0.033, and p=0.738), and other patients' characteristics. Conclusions. In patients with T2DM there is no correlation between S100B serum levels and newly detected mild depressive symptoms. The brain biochemistry pathways of depression in T2DM warrant further investigation in a larger scale population.
Highlights
Depression is a common comorbid condition in patients with Type 2 Diabetes mellitus (T2DM) [1] with important clinical significance
It is recently discovered that the effect of antidepressant medicine could be the upregulation of neurogenesis especially in the adult hippocampus, which can be expressed by S100 calcium-binding protein b (S100B) values [14], supporting the hypothesis that S100B seems to be a marker of antidepressive treatment outcomes
In this study we examined for differences in serum S100B concentrations between subjects with and without depressive symptoms in a cohort of patients with T2DM and for potential associations between S100B serum levels and metabolic as well as depression parameters
Summary
Depression is a common comorbid condition in patients with Type 2 Diabetes mellitus (T2DM) [1] with important clinical significance. S100 calcium-binding protein b (S100B) is a molecule deriving from glia with a specified role in glial disorder. It appears to have important activity in cellular shape and Depression Research and Treatment intracellular communication [8]. In the general population the loss of neuroplasticity due to glial cells alterations supports the neurodegenerative hypothesis of depression [9]. T2DM is associated apart from inflammation, with impaired neurogenesis and decreased synaptic plasticity [15], the clinical significance of S100B is yet to be investigated in depressive patients with T2DM. In this study we examined for differences in serum S100B concentrations between subjects with and without depressive symptoms in a cohort of patients with T2DM and for potential associations between S100B serum levels and metabolic as well as depression parameters
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
