Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism

Nutr Rev. 2005 May;63(5):133-57. doi: 10.1301/nr.2005.may.133-157.

Abstract

Fructose intake and the prevalence of obesity have both increased over the past two to three decades. Compared with glucose, the hepatic metabolism of fructose favors lipogenesis, which may contribute to hyperlipidemia and obesity. Fructose does not increase insulin and leptin or suppress ghrelin, which suggests an endocrine mechanism by which it induces a positive energy balance. This review examines the available data on the effects of dietary fructose on energy homeostasis and lipid/carbohydrate metabolism. Recent publications, studies in human subjects, and areas in which additional research is needed are emphasized.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Beverages
  • Diabetes Mellitus, Type 2 / metabolism
  • Diabetes Mellitus, Type 2 / physiopathology
  • Energy Metabolism / drug effects
  • Energy Metabolism / physiology
  • Fructose / administration & dosage
  • Fructose / metabolism*
  • Fructose / pharmacology
  • Ghrelin
  • Glucose / metabolism
  • Humans
  • Hyperlipidemias / etiology
  • Insulin / metabolism
  • Insulin Resistance / physiology
  • Leptin / metabolism
  • Obesity / metabolism*
  • Peptide Hormones / metabolism

Substances

  • Ghrelin
  • Insulin
  • Leptin
  • Peptide Hormones
  • Fructose
  • Glucose