Figure 1.

Mechanisms of metabolic syndrome (MS) pathophysiology. MS is a result of a metabolic imbalance which involves alterations in different tissues and a variety of molecules. (1) Insulin resistance is accompanied by (2) a low-grade inflammation in the adipose tissue characterized by reduction of adipokines such as adiponectin, enhanced levels of leptin and resistin, accumulation of inflammatory cells in the adipose tissue, paralleled with high levels of cytokines/chemokines and reactive oxygen species. Alterations of the central (hypothalamus and the brainstem) and peripheral mechanisms of hunger and satiety occur (3). All these events contribute towards (4) decreased energy expenditure, hyperglycaemia and dyslipidaemia, increasing the risk for type 2 diabetes and cardiovascular diseases. Nutrient absorption (5) and the gut microbiota play key roles in the modulation of MS, aiding the connection between the brain and metabolic tissues. TG—triglycerides; VLDL—very low-density lipoprotein; CCK—cholecystokinin; Ecs—estrogens; GLP-1—glucagon-like peptide-1; GIP—gastric inhibitor peptide; TNFα—tumour necrosis factor α; IL-6—interleukin-6; MCP-1—macrophage chemotatic protein-1.