Abstract
Aims: Obesity is associated with a chronic systemic low-grade inflammatory state. Markers of inflammation such as TNF-α are linked with increased risk for insulin resistance and type 2 diabetes. The objective of the present study was to dissect the molecular mechanisms that may regulate TNF-α-induced insulin resistance in human adipose tissue. Methods: We analyzed the impact of TNF-α on glucose uptake and insulin action in human visceral and sc adipocytes. The contribution of different intracellular signaling pathways on metabolic effects of TNF-α and the reversal of some of these effects with nuclear receptor agonists were also studied. Results: TNF-α per se increased glucose transporter-4 translocation to the plasma membrane and glucose uptake by activating the AMP-activated protein kinase/AS160 pathway in both visceral and sc adipocytes. Nevertheless, this cytokine induced an insulin-resistant state in visceral adipocytes by impairing insulin-stimulated glucose uptake and insulin signaling at the insul...
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