New research published in Molecular Psychiatry suggests that major depressive disorder (MDD) is also linked to increased inflammation glucose homeostasis and adipose tissue-associated insulin resistance (AAI-INS) in fat cells. Importantly these findings support a direct bearing of the disorder on the origin of diabetes in leukocytes and suggest possible therapeutic strategies for this relatively understudied condition. The study is led by Dr Marco Binschtein of the Department of Biomedical Sciences and the Novo Nordisk Foundation Center for Protein Research in collaboration with the SSM Universitat Jaume I and the Federal University of Rio de Janeiro.

According to the World Health Organizations European Centre for Disease Prevention and Control 5. 5 million people were affected by MDD in 2016 representing a 31 increase over the previous year. However the most common form of the disease short-term depression of interest is also associated with inflammation and insulin resistance in adipose tissues where increased body fat occurs as a consequence. Elevated fasting blood glucose levels play a central role in the etiology of MDD and its prevalence increases with the severity and duration of an individuals symptoms. In its current form MDD is a type of affective disorder characterized by marked disability psychosocial problems and impairment in daily activities.

An estimated 15 of the worlds population is diagnosed annually with MDD which accounts for approximately 1. 8 million MDD patients in the Developing Diseases Programme of the WHO. Recently studies have begun to shed light on how where and why MDD develops into a chronic inflammatory state. These studies reveal a link between inflammation oxidative stress and metabolic dysfunction that are both suspected to play a role in MDD pathogenesis in humans. The methodology used to identify the relevant environmental risks has been a great challenge in part because it is difficult to separate between looking for physiological effects of inflammation and disease progression.

In the present study Dr Binschteins group chose to develop quantitative quantitative assays that are a little bit more realistic in their ability to measure risk factors associated with MDD. To build the quantitative assay they studied a large group of patients with short-term and chronic MDD. In addition to the treatment of a lower depressive state the participants also completed certain developmental tasks or underwent magnetic resonance spectroscopy data analysis. Quantitative tests are very sensitive in monitoring gene expression. Using their quantitative assays the team identified gene expression changes in fat cells as a marker for MDD.

Their results revealed a clear relationship between the severity of depressive symptoms fasting blood glucose levels and both inflammation and glucose homeostasis.

These findings suggest that inflammation and glucose homeostasis could shape biochemical phenotype as well as the microbe fate in MDD. Moreover we also confirmed that mild depression can and does alter microbe diversity and gene expression in adipose tissue providing new information about the impact of this condition on both inflammatory and diabetic patients.


In addition the group created a mouse model for MDD that mimics most of the controls. They overcome the difficulty of directly comparing the animals from different carriers to the best-performing animals in order to achieve complete normalization of gene expression. Their results were highly significant in demonstrating good statistical effectiveness as indicated by Figure 1.