@article{2541,
  keywords = {Animals, Glucose, Liver, Models, Biological, Mice, Inbred C57BL, Metabolome, Isotope Labeling, Feeding Behavior, Microbiota, Carboxylic Acids, Dietary Carbohydrates, Fructose, Intestine, Small},
  author = {Cholsoon Jang and Sheng Hui and Wenyun Lu and Alexis Cowan and Raphael Morscher and Gina Lee and Wei Liu and Gregory Tesz and Morris Birnbaum and Joshua Rabinowitz},
  title = {The Small Intestine Converts Dietary Fructose into Glucose and Organic Acids.},
  abstract = {<p>Excessive consumption of sweets is a risk factor for metabolic syndrome. A major chemical feature of sweets is fructose. Despite strong ties between fructose and disease, the metabolic fate of fructose in mammals remains incompletely understood. Here we use isotope tracing and mass spectrometry to track the fate of glucose and fructose carbons in\&nbsp;vivo, finding that dietary fructose is cleared by the small intestine. Clearance requires the fructose-phosphorylating enzyme ketohexokinase. Low doses of fructose are \&sim;90\% cleared by the intestine, with only trace fructose but extensive fructose-derived glucose, lactate, and glycerate found in the portal blood. High doses of fructose (\&ge;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. We propose that the small intestine shields the liver from otherwise toxic fructose exposure.</p>
},
  year = {2018},
  journal = {Cell Metab},
  volume = {27},
  pages = {351-361.e3},
  month = {02/2018},
  issn = {1932-7420},
  doi = {10.1016/j.cmet.2017.12.016},
  language = {eng},
}