Framing insulin resistance: impact on liver and peripheral tissues
(2011) 16th international symposium on Cells of the Hepatic Sinusoid — Location: Florence, Italy (22.September.2011)
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- Abstract
- Insulin resistance is defined by the impaired responsiveness of target organs to circulating insulin translated as impaired inhibition of hepatic glucose production, decreased peripheral glucose uptake, leading up to hyperglycemia, hyperinsulinemia and evolution towards type2 diabetes, and increased FFA release by the adipose tissue, a strong contributor to fatty liver. Insulin resistance is a hallmark of fatty liver. The fatty liver is a prominent producer of CV risk factors and predicts cardiovascular events Chronic low grade inflammation is associated with obesity. The mechanism for coupling of nutrient entry to inflammatory signals within metabolic tissues is incompletely resolved but likely involves lipids species by themselves (lipotoxicity, lipid metabolites, specific activation of signal transduction pathways, ER stress) and activation of the innate immunity. This has an inhibitory effect on insulin signaling through inflammatory kinases (JNK, IKK, PKR ). The immune system directly, secondarily or via amplification loops propagate signals to other tissues to induce a systemic inflammatory response, influencing the development of obesity and its systemic complications. We provide data supporting that the metabolic and secretory profile of the liver under conditions of increased lipid load may be a strong contributor of the malfunction of peripheral tissues, particularly at the onset of obesity-induced disorders.
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Leclercq, I. (2011). Framing insulin resistance: impact on liver and peripheral tissues. 16th international symposium on Cells of the Hepatic Sinusoid, Florence, Italy. https://hdl.handle.net/2078.5/59242