PMC

Stress and microRNA expression. A model in which the lack of physical activity, disruption of circadian rhythm, and psychological and environmental stress deregulates the expression of miRs which directly or indirectly through inflammation disrupts adipogenesis and contributes to the development of obesity and associated disorders.

The interaction between different stress factors and pathophysiological processes in obesity. Behaviour and physiological and environmental stress conditions impair epigenetic control mechanisms resulting in exacerbation of inflammation that is already increased in adipocytes and circulatory and tissue inflammatory cells in obese subjects.

Schematic representation of the central role of inflammation in obesity-induced disorders. The inflammatory state, associated with excessive caloric intake during obesity induces adipose tissue remodelling, oxidative stress, and insulin resistance, associated with an increased risk of developing metabolic syndrome, type 2dibetes, and cardiovascular diseases.

Low-grade chronic inflammation and oxidative stress in adipose tissue during obesity. The excessive accumulation of adipose tissue during obesity is characterized by the recruitment of immune cells. Activated T cells and chemokines induce monocyte migration into adipose tissues where they differentiate into proinflammatory M1 macrophages. The interaction between activated T cells, macrophages, and dysfunctional adipocytes results in a dysregulated adipokine and exosome-like vesicle production causing insulin resistance (IR). Adipose tissue hypoxia during obesity is associated with ROS and ox-LDL production, and foam cell formation. In addition, hypoxia and increased oxidative stress induce apoptosis of adipocytes contributing to insulin resistance.