[Metabolic or immunometabolic syndrome?]

Area of Science:

• Immunology
• Metabolic Disorders
• Cardiovascular Disease

Background:

• Insulin resistance and metabolic syndrome pathogenesis understanding has evolved.
• Shared risk factors for cardiovascular disease, type 2 diabetes, obesity, and dyslipidemia prompt investigation into their pathophysiology.
• Growing evidence links inflammatory markers to metabolic syndrome components.

Purpose of the Study:

• To investigate if an inflammatory state is a fundamental factor in metabolic syndrome development, similar to its role in atherosclerosis.
• To explore the hypothesis that chronic, low-grade inflammation underlies metabolic syndrome and its complications.

Main Methods:

• Review of studies correlating inflammatory markers (e.g., CRP, fibrinogen, leptin, TNF-alpha) with metabolic syndrome variables.
• Analysis of associations between inflammatory mediators and obesity, a key metabolic syndrome component.
• Examination of the hypothesis linking chronic immune system activation to metabolic and neuroendocrine alterations.

Main Results:

• Statistically significant correlations observed between inflammatory markers and metabolic syndrome diseases.
• Strong associations found between inflammatory mediators and obesity, a primary metabolic syndrome variable.
• Evidence suggests chronic activation of the innate immune system contributes to both atherosclerosis and insulin resistance.

Conclusions:

• A chronic, mild inflammatory state is a likely underlying factor for metabolic syndrome and its complications.
• Metabolic syndrome may be conceptualized as an immune-metabolic disease, resulting from chronic immune system activation.
• Daily stressors may initiate immune and neuroendocrine alterations, leading to metabolic disorders.