Insulin resistance in non-diabetic patients with non-alcoholic fatty liver disease: sites and mechanisms

By E. Bugianesi, Amalia Gastaldelli, E. Vanni, R. Gambino, M. Cassader, S. Baldi, V. Ponti, G. Pagano, E. Ferrannini, M. Rizzetto. Diabetologia, 2005

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Hepatic lipotoxicity and the pathogenesis of nonalcoholic steatohepatitis: The central role of nontriglyceride fatty acid metabolites (2010, background): “Fructose enters the glycolytic pathway to fatty acid synthesis downstream from phosphofructokinase, the rate-limiting enzyme for this pathway, and thus fructose provides an unregulated source of acetyl-CoA as the substrate for DNL.84,85 Studies in mice have confirmed the importance of dietary sugars”
Non-Alcoholic Fatty Liver Disease (NAFLD) and Its Connection with Insulin Resistance, Dyslipidemia, Atherosclerosis and Coronary Heart Disease (2013, positive): “Increased CRP promotes inflammation and accelerates atherosclerosis by increasing the expression of plasminogen activator inhibitor-1 and adhesion molecules in endothelial cells, inhibiting nitric oxide formation and increasing LDL uptake into macrophages [51].”
Insulin resistance drives hepatic de novo lipogenesis in nonalcoholic fatty liver disease. (2019, background): “Data from a series of studies have shown that the rate of VLDLTG secretion is increased (2, 7, 8) and hepatic fatty acid oxidation is likely normal or increased in people with NAFLD (9-11), demonstrating that an increase in IHTG production rather than a decrease in IHTG mobilization is the primary m”