Various translational studies have identified the differential role of saturated and unsaturated fatty acids and their effects at cardiovascular level. On the other hand, activated NF-κB also might be implicated in JNK-1/2 activation and induces insulin resistance in several tissues. De que protege san benito Activator#ICAM-1), monocyte chemotactic protein 1 (MCP-1), and plasminogen activator inhibitor-1 (PAI-1). Moreover, NF-κB also regulates the expression of genes involved in the early and late atherosclerotic process and its instability, such as endothelial nitric oxide synthase (eNOS), adhesion molecules ( e.g. IL-6 strongly correlates with insulin resistance and type 2 diabetes and its plasma levels are increased in patients with obesity and type 2 diabetes. Once activated, NF-κB regulates the expression of multiple inflammatory mediators, including IL-6, TNF-α and other factors implicated in the metabolic alterations. Both mechanisms lead to the activation of the proinflammatory transcription factor nuclear factor-kappa B (NF-κB), which has been linked to fatty acid-induced impairment of insulin action in skeletal muscle. Elevated saturated FFAs can induce inflammation and insulin resistance, through several mechanisms including diacylglycerol-mediated activation of protein kinase Cθ and activation of Toll-like receptors (TLR). By contrast, mono- or poly-unsaturated FFAs (MUFAs or PUFAs) protects against SFAs. palmitate) induce inflammatory responses and cause insulin resistance in peripheral tissues. Elevated circulating levels of saturated free fatty acids (SFAs e.g.
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