Cellular Stresses and Stress Responses in the Pathogenesis of Insulin Resistance

Figure 3

Psychological stress-dependent pathways to oxidative and nitrosative stresses. Psychological stress activates the renin-angiotensin-aldosterone system (RAAS), the hypothalamic-pituitary-adrenal axis (HPA), and the sympathetic adrenomedullary system (SAS), leading to increased availability of angiotensin II (Ang II), aldosterone, glucocorticoids, catecholamines, and free fatty acids which induce oxidative and nitrosative stresses in insulin target cells [109, 117–120, 127, 128]. Glucocorticoids and aldosterone promote de novo ceramide synthesis in endothelial cells and may thereby contribute to plasma ceramides [111, 121–123]. Glucocorticoids also increase colon epithelial barrier permeability and thus increase circulating LPS [124–126]. Angiotensin II, glucocorticoids, aldosterone, and catecholamines upregulate Nox activity in various insulin target cells [105, 110, 130, 132].