title: Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance.
abstract: OBJECTIVE
  Based on interim results from an ongoing study, we have reported that consumption of a high-fructose diet, but not a high-glucose diet, promotes the development of three of the pathological characteristics associated with metabolic syndrome: visceral adiposity, dyslipidemia, and insulin resistance. From these results and a review of the current literature, we present two potential sequences of events by which fructose consumption may contribute to metabolic syndrome.
  
  
  RESULTS
  The earliest metabolic perturbation resulting from fructose consumption is postprandial hypertriglyceridemia, which may increase visceral adipose deposition. Visceral adiposity contributes to hepatic triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance by increasing the portal delivery of free fatty acids to the liver. With insulin resistance, VLDL production is upregulated and this, along with systemic free fatty acids, increase lipid delivery to muscle. It is also possible that fructose initiates hepatic insulin resistance independently of visceral adiposity and free fatty acid delivery. By providing substrate for hepatic lipogenesis, fructose may result in a direct lipid overload that leads to triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance.
  
  
  CONCLUSIONS
  Our investigation and future studies of the effects of fructose consumption may help to clarify the sequence of events leading to development of metabolic syndrome.
authors.affiliation: Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, California 95616, USA.
authors.forename: Kimber L
authors.initials: KL
authors.lastname: Stanhope
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Havel
mesh_terms: D050171:Dyslipidemias / Q000097:blood / Q000139:chemically induced* / Q000503:physiopathology*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005632:Fructose / Q000494:pharmacology / Q000502:physiology*; D006801:Humans; D007333:Insulin Resistance; D050152:Intra-Abdominal Fat / Q000187:drug effects* / Q000378:metabolism; D013549:Sweetening Agents / Q000494:pharmacology
chemical_list: D005230:Fatty Acids, Nonesterified; D013549:Sweetening Agents; D005632:Fructose