Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism.
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.
Havel
Peter J
PJ
Department of Nutrition, University of California, One Shields Avenue, Davis, CA 95616, USA. pjhavel@ucdavis.edu
D001628:Beverages; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism / Q000503:physiopathology; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology; D005632:Fructose / Q000008:administration & dosage / Q000378:metabolism* / Q000494:pharmacology; D054439:Ghrelin; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006949:Hyperlipidemias / Q000209:etiology; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology; D020738:Leptin / Q000378:metabolism; D009765:Obesity / Q000378:metabolism*; D036361:Peptide Hormones / Q000378:metabolism
D054439:Ghrelin; D007328:Insulin; D020738:Leptin; D036361:Peptide Hormones; D005632:Fructose; D005947:Glucose