In the liver, fructose increases triacylglycerol synthesisand VLDL secretion, leading to hypertriacylglycerolemia—andincreased LDL cholesterol—which canbe regarded as potentially atherogenic (Chapter 26). Inaddition, acute loading of the liver with fructose, as canoccur with intravenous infusion or following very highfructose intakes, causes sequestration of inorganic phosphatein fructose 1-phosphate and diminished ATPsynthesis. As a result there is less inhibition of de novopurine synthesis by ATP and uric acid formation is increased, causing hyperuricemia, which is a cause of gout(Chapter 34).
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