Sugar, Sugar . . . Not So Sweet for the Liver Miriam B. Vos  Gastroenterology  Volume 153, Issue 3, Pages 642-645 (September 2017) DOI: 10.1053/j.gastro.2017.07.029 Copyright © 2017 AGA Institute Terms and Conditions

Figure 1 Fructose metabolism in NAFLD. Fructose is quickly transported from the gut to the liver through portal blood. Once in the liver, it is up-taken into hepatocytes rapidly, because of 10 fold higher levels in portal blood compared to other tissues and first pass clearance metabolism. In the liver, hepatic fat is derived from hepatic de novo lipogenesis (DNL), from the diet or from esterification of free fatty acids (FFA). Fructose promotes DNL which is already increased in NAFLD, and inhibits β oxidation, promoting accumulation of hepatic steatosis. Increased triglyceride from DNL is exported out of the liver through large very low density lipoproteins (VLDL), which contributes to dyslipidemia, increased low density lipoprotein (LDL) and development of atherosclerosis. The cycle of dysfunction continues as lipoprotein remnants of the large VLDL and FFA from visceral and subcutaneous adipose tissue are channeled back towards the liver contributing to lipid overload. Gastroenterology 2017 153, 642-645DOI: (10.1053/j.gastro.2017.07.029) Copyright © 2017 AGA Institute Terms and Conditions