scholarly journals Central and Peripheral Inflammation Link Metabolic Syndrome and Major Depressive Disorder

Physiology ◽  
2019 ◽  
Vol 34 (2) ◽  
pp. 123-133 ◽  
Author(s):  
Kenny L. Chan ◽  
Flurin Cathomas ◽  
Scott J. Russo
Keyword(s):  
Metabolic Syndrome ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Chronic Stress ◽  
Immune Cells ◽  
Low Grade ◽  
Major Depressive ◽  
Metabolic Dysregulation ◽  
Critical Areas ◽  
Behavioral Abnormalities

Metabolic syndrome and major depression are two of the most common and debilitating disorders worldwide, occurring with significant rates of comorbidity. Recent studies have uncovered that each of these conditions is associated with chronic, low-grade inflammation. This is characterized by increased circulating pro-inflammatory cytokines, altered leukocyte population frequencies in blood, accumulation of immune cells in tissues including the brain, and activation of these immune cells. Cytokines that become elevated during obesity can contribute to the progression of metabolic syndrome by directly causing insulin resistance. During chronic stress, there is evidence that these cytokines promote depression-like behavior by disrupting neurotransmitter synthesis and signal transduction. Animal models of obesity and depression have revealed a bi-directional relationship whereby high-fat feeding and chronic stress synergize and exacerbate metabolic dysregulation and behavioral abnormalities. Although far from conclusive, emerging evidence suggests that inflammation in the central and peripheral immune system may link metabolic syndrome to major depressive disorder. In this review, we will synthesize available data supporting this view and identify critical areas for future investigation.

Metabolic syndrome in subjects with bipolar disorder and major depressive disorder in a current depressive episode: Population-based study

2017 ◽  
Vol 92 ◽  
pp. 119-123 ◽  
Author(s):  
Fernanda Pedrotti Moreira ◽  
Karen Jansen ◽  
Taiane de Azevedo Cardoso ◽  
Thaíse Campos Mondin ◽  
Pedro Vieira da Silva Magalhães ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Bipolar Disorder ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Depressive Episode ◽  
Population Based ◽  
Major Depressive ◽  
Population Based Study ◽  
A Current

Shared Transcriptional Signatures in Major Depressive Disorder and Mouse Chronic Stress Models

2020 ◽  
Vol 87 (9) ◽  
pp. S222
Author(s):  
Joseph Scarpa ◽  
Mena Fatma ◽  
Yong-Hwee E. Loh ◽  
Said Romaric Traore ◽  
Théo Stefan ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Chronic Stress ◽  
Major Depressive ◽  
Stress Models

scholarly journals Characterization of GABAergic Marker Expression in the Chronic Unpredictable Stress Model of Depression

2017 ◽  
Vol 1 ◽  
pp. 247054701772045 ◽  
Author(s):  
Mounira Banasr ◽  
Ashley Lepack ◽  
Corey Fee ◽  
Vanja Duric ◽  
Jaime Maldonado-Aviles ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Prefrontal Cortex ◽  
Depressive Disorder ◽  
Protein Expression ◽  
Neuropeptide Y ◽  
Chronic Stress ◽  
Gabaergic Interneurons ◽  
Chronic Unpredictable Stress ◽  
Major Depressive

Background Evidence continues to build suggesting that the GABAergic neurotransmitter system is altered in brains of patients with major depressive disorder. However, there is little information available related to the extent of these changes or the potential mechanisms associated with these alterations. As stress is a well-established precipitant to depressive episodes, we sought to explore the impact of chronic stress on GABAergic interneurons. Methods Using western blot analyses and quantitative real-time polymerase chain reaction, we assessed the effects of five-weeks of chronic unpredictable stress exposure on the expression of GABA-synthesizing enzymes (GAD65 and GAD67), calcium-binding proteins (calbindin, parvalbumin, and calretinin), and neuropeptides co-expressed in GABAergic neurons (somatostatin, neuropeptide Y, vasoactive intestinal peptide, and cholecystokinin) in the prefrontal cortex and hippocampus of rats. We also investigated the effects of corticosterone and dexamethasone exposure on these markers in vitro in primary cortical and hippocampal cultures. Results We found that chronic unpredictable stress induced significant reductions of GAD67 protein levels in both the prefrontal cortex and hippocampus of chronic unpredictable stress-exposed rats but did not detect changes in GAD65 protein expression. Similar protein expression changes were found in vitro in cortical neurons. In addition, our results provide clear evidence of reduced markers of interneuron population(s), namely somatostatin and neuropeptide Y, in the prefrontal cortex, suggesting these cell types may be selectively vulnerable to chronic stress. Conclusion Together, this work highlights that chronic stress induces regional and cell type-selective effects on GABAergic interneurons in rats. These findings provide additional supporting evidence that stress-induced GABA neuron dysfunction and cell vulnerability play critical roles in the pathophysiology of stress-related illnesses, including major depressive disorder.

scholarly journals Metabolic syndrome and metabolic abnormalities in patients with major depressive disorder: a meta-analysis of prevalences and moderating variables

2013 ◽  
Vol 44 (10) ◽  
pp. 2017-2028 ◽  
Author(s):  
D. Vancampfort ◽  
C. U. Correll ◽  
M. Wampers ◽  
P. Sienaert ◽  
A. J. Mitchell ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Geographical Area ◽  
Medical Subject Headings ◽  
Prevalence Odds Ratio ◽  
Major Depressive ◽  
Cardiovascular Morbidity And Mortality ◽  
Co Morbidity ◽  
Antidepressant Use

BackgroundIndividuals with depression have an elevated risk of cardiovascular disease (CVD) and metabolic syndrome (MetS) is an important risk factor for CVD. We aimed to clarify the prevalence and correlates of MetS in persons with robustly defined major depressive disorder (MDD).MethodWe searched Medline, PsycINFO, EMBASE and CINAHL up until June 2013 for studies reporting MetS prevalences in individuals with MDD. Medical subject headings ‘metabolic’ OR ‘diabetes’ or ‘cardiovascular’ or ‘blood pressure’ or ‘glucose’ or ‘lipid’ AND ‘depression’ OR ‘depressive’ were used in the title, abstract or index term fields. Manual searches were conducted using reference lists from identified articles.ResultsThe initial electronic database search resulted in 91 valid hits. From candidate publications following exclusions, our search generated 18 studies with interview-defined depression (n = 5531, 38.9% male, mean age = 45.5 years). The overall proportion with MetS was 30.5% [95% confidence interval (CI) 26.3–35.1] using any standardized MetS criteria. Compared with age- and gender-matched control groups, individuals with MDD had a higher MetS prevalence [odds ratio (OR) 1.54, 95% CI 1.21–1.97, p = 0.001]. They also had a higher risk for hyperglycemia (OR 1.33, 95% CI 1.03–1.73, p = 0.03) and hypertriglyceridemia (OR 1.17, 95% CI 1.04–1.30, p = 0.008). Antipsychotic use (p < 0.05) significantly explained higher MetS prevalence estimates in MDD. Differences in MetS prevalences were not moderated by age, gender, geographical area, smoking, antidepressant use, presence of psychiatric co-morbidity, and median year of data collection.ConclusionsThe present findings strongly indicate that persons with MDD are a high-risk group for MetS and related cardiovascular morbidity and mortality. MetS risk may be highest in those prescribed antipsychotics.

scholarly journals Molecular mechanism of reward treatment ameliorating chronic stress-induced depressive-like behavior assessed by sequencing miRNA and mRNA in medial prefrontal cortex

2020 ◽  
Author(s):  
Tingting An ◽  
Zhenhua Song ◽  
Jin-Hui Wang
Keyword(s):  
Major Depressive Disorder ◽  
Prefrontal Cortex ◽  
Depressive Disorder ◽  
Molecular Mechanism ◽  
Chronic Stress ◽  
Medial Prefrontal Cortex ◽  
Differentially Expressed ◽  
Mild Stress ◽  
Major Depressive ◽  
Differentially Expressed Mirnas

Abstract Background Major depressive disorder (MDD) is a disease that seriously endangers human health and mental state. Chronic stress and lack of reward may reduce the function of the brain's reward circuits, leading to major depressive disorder. The effect of reward treatment on chronic stress-induced depression-like behaviors and its molecular mechanism in the brain remain unclear.Methods Mice were divided into the groups of control, chronic unpredictable mild stress (CUMS), and CUMS-companion. Mice of CUMS group was performed by CUMS for 4 weeks, and CUMS-companion group was treated by CUMS accompanied with companion. The tests of sucrose preference, Y-maze, and forced swimming were conducted to assess depression-like behaviors or resilience. High-throughput sequencing was used to analyze mRNA and miRNA profiles in the medial prefrontal cortex harvested from control, CUMS-MDD (mice with depression-like behaviors in CUMS group), Reward-MDD (mice with depression-like behaviors in CUMS-companion group), CUMS-resilience (resilient mice in CUMS group), Reward-resilience (resilient mice in CUMS-companion group) mice.Results The results provided evidence that accompanying with companion ameliorated CUMS-induced depression-like behaviors in mice. 45 differentially expressed genes (DEGs) are associated with depression-like behaviors, 8 DEGs are associated with resilience and 59 DEGs are associated with nature reward (companion) were identified. Furthermore, 196 differentially expressed miRNAs were found to be associated with companion. Based on the differentially expressed miRNAs and DEGs data, miRNA-mRNA network was established to be associated with companion.Conclusion Taken together, our data here provided a method to ameliorate depression-like behaviors, and numerous potential drug targets for the prevention or treatment of depression.

scholarly journals Major Depressive Disorder: a possible typisation according to serotonin, inflammation, and metabolic syndrome

2021 ◽  
pp. 1-24
Author(s):  
Ante Silić ◽  
Jakša Vukojević ◽  
Vjekoslav Peitl ◽  
Marc De Hert ◽  
Dalibor Karlović
Keyword(s):  
Metabolic Syndrome ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Clinical Laboratory ◽  
Major Depressive ◽  
Cross Sectional ◽  
High Blood Glucose ◽  
The Metabolic Syndrome ◽  
Platelet Serotonin ◽  
Depressive Episodes

Abstract Objective: Major depressive disorder (MDD) is closely related to obesity, inflammation, and insulin resistance, all together being etiologically linked to metabolic syndrome development. The depressive disorder has a neuroendocrinological component, co-influencing the metabolic syndrome, while metabolic syndrome (MetS) is characterized by increased cytokine levels, which are known to cause a depressed mood. This study aimed to establish biological subtypes of the depressive disorder based on researched clinical, laboratory, and anthropometric variables. Methods: We performed a cross-sectional study on a sample of 293 subjects (145 suffering from a depressive disorder and 148 healthy controls). Results were analyzed with multivariate statistical methods as well as with cluster and discriminant analysis. In order to classify depressive disorder on the grounds of laboratory, anthropometric, and clinical parameters, we performed cluster analysis, which resulted in three clusters. Results: The first cluster is characterized by low platelet serotonin, high cortisol levels, high blood glucose levels, high triglycerides levels, high HAMD score, increased waist circumference, high CRP values, and a high number of previous depressive episodes, was named Combined (Metabolic) depression. The inflammatory depression cluster is defined with average platelet serotonin values, normal cortisol, and all other parameter levels, except for increased IL-6 levels. The serotoninergic depression cluster is characterized by markedly low platelet serotonin, and all other parameters are within the normal range. Conclusions: From a biological point of view, depressive disorder is not uniform, and as such, these findings suggest potential clinically useful and generalizable biological subtypes of depressive disorder.

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