Fructose stimulated de novo lipogenesis is promoted by inflammation

Excessive fructose intake causes dysbiosis and tight-junction proteins downregulation, resulting in intestinal-barrier deterioration and low-grade endotoxaemia. Fructose consumption stimulates hepatosteatosis and, when combined with other risk factors, can cause steatohepatitis and even hepatocellular carcinoma. It is well established...
PUBLISHED IN: Nature Metabolism 2020

Commentary

Excessive fructose intake causes dysbiosis and tight-junction proteins downregulation, resulting in intestinal-barrier deterioration and low-grade endotoxaemia. Fructose consumption stimulates hepatosteatosis and, when combined with other risk factors, can cause steatohepatitis and even hepatocellular carcinoma. It is well established that fructose is a more effective inducer of hepatic de novo lipogenesis than glucose is. However, the exact mechanism by which fructose preferentially drives de novo lipogenesis, other than its ketohexokinase-dependent conversion to acetyl-CoA via fructolysis, remained obscure.

J. Todoric et al. (Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California San Diego, La Jolla, California and Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria) have shown that inflammation associated with fructose-induced barrier deterioration induces hepatic fructose-stimulated de novo lipogenesis, NASH development and hepatocellular carcinoma.

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Dr. D. Beard

DR. D. BEARD is specialist of Nash Pathology

Articles: 191

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