Obesity and Stroke: Does the Paradox Apply for Stroke?

Figures

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  Fig. 1.. Increased activity of IkB/NFkB as the basis of the chronic inflammation and insulin resistance in type 2 diabetes. Intracellular fatty acyl-CoA levels found in insulin resistance and lipotoxicity, in correlation to the subsequent activation of the enzyme IkB kinase (via inflammatory factors such as fatty acyl-CoAs), will phosphorylate IkB, causing the release of NFkB (upon the polyubiquitination and degradation of IkB), which enters the nucleus where it is responsible for inflammation, cell proliferation and atherogenesis by the stimulation of inflammatory cytokines, growth factors, and iNOS, which in turn will stimulate TNFα, IL-6, and PKC, which will impede insulin signaling by serine phosphorylation of IRS-1 ultimately, causing insulin resistance. Therefore, the increased activity of IkB/NFkB will not only instigate inflammation but also further aid and boost atherogenesis. The MAP kinase pathway is responsible for the insulin-stimulated glucose impaired metabolism and for this reason, related to cardiovascular diseases. FACoA, Fatty acyl-CoA; IkB, Inhibitor kβ; IL1 and IL6, Interleukins 1 and 6; IRS, Insulin Receptor Substitute 1; MAP, Mitogen-Activated Protein; NFkB, Nuclear…

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  Fig. 2.. The adiposity and lipotoxicity in chronic disease. Adapted and modified from the article of Heymsfield and Wadden (N Engl J Med 2017;376:254-266) [57].