Fructose

From Biohacking Wiki

Fructose vs Glucose Metabolism

the unique aspect of fructose compared to glucose is that when fructose is metabolized there is a transient decrease in intracellular phosphate and ATP levels associated with nucleotide turnover and uric acid generation. This fall in ATP level induces a series of reactions, including a transient block in protein synthesis, an induction in oxidative stress, and mitochondrial dysfunction that turn out to have a key role in fructose-mediated effects [1]

24-h postprandial triglyceride (TG) profiles were increased after 10 weeks of fructose consumption, but tended to decrease after glucose consumption. The rate of hepatic de novo lipogenesis (DNL) was higher and postheparin lipoprotein lipase activity (LPL) was lower in subjects consuming fructose compared with those consuming glucose, suggesting that both increased very low density lipoprotein (VLDL) secretion and decreased TG clearance contributed to the effects of fructose to increase postprandial triglycerides. Fasting plasma concentrations of low density lipoprotein (LDL) cholesterol, apolipoprotein B (apoB), small dense LDL (sdLDL), oxidized LDL and postprandial concentrations of remnant-like particle lipoprotein (RLP)-TG and of RLP-cholesterol were also significantly increased in subjects consuming fructose-sweetened beverages, but not in subjects consuming glucose beverages [2]

Thus, consumption of 25% of energy requirements from fructose for 10 weeks, results in increased visceral adiposity, lipid dysregulation, and decreased insulin sensitivity, all of which have been associated with increased risk for cardiovascular disease and type 2 diabetes[3]

Low doses of fructose are ∼90% cleared by the intestine (taken in by Glut5), with only trace fructose but extensive fructose-derived glucose, lactate, and glycerate found in the portal blood. High doses of fructose (≥1 g/kg) overwhelm intestinal fructose absorption and clearance, resulting in fructose reaching both the liver and colonic microbiota. Intestinal fructose clearance is augmented both by prior exposure to fructose and by feeding [4]