The Small Intestine Converts Dietary Fructose into Glucose and Organic Acids Academic Article uri icon

Overview

MeSH Major

  • Autophagy
  • Drosophila Proteins
  • Drosophila melanogaster
  • Protein-Serine-Threonine Kinases
  • Ribosomal Protein S6 Kinases

abstract

  • 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 vivo, finding that dietary fructose is cleared by the small intestine. Clearance requires the fructose-phosphorylating enzyme ketohexokinase. Low doses of fructose are ∼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 (≥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.

publication date

  • February 6, 2018

Research

keywords

  • Academic Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1016/j.cmet.2017.12.016

PubMed ID

  • 29414685

Additional Document Info

start page

  • 351

end page

  • 361.e3

volume

  • 27

number

  • 2