title: Effects of dietary fat modification on skeletal muscle fatty acid handling in the metabolic syndrome.
abstract: OBJECTIVE
  In the metabolic syndrome (MetS), increased fat storage in 'nonadipose' tissues such as skeletal muscle may be related to insulin resistance ('lipid overflow' hypothesis). The objective of this study was to examine the effects of dietary fat modification on the capacity of skeletal muscle to handle dietary and endogenous fatty acids (FAs).
  
  
  METHODS
  In total, 29 men with the MetS were randomly assigned to one of four diets for 12 weeks: a high-fat saturated fat diet (HSFA, n=6), a high-fat monounsaturated fat diet (HMUFA, n=7) and two low-fat high-complex carbohydrate diets supplemented with (LFHCCn-3, n=8) or without (LFHCC, n=8) 1.24 g per day docosahexaenoic and eicosapentaenoic acid. Fasting and postprandial skeletal muscle FA handling was examined by measuring arteriovenous concentration differences across the forearm muscle. [(2)H(2)]-palmitate was infused intravenously to label endogenous triacylglycerol (TAG) and free fatty acids in the circulation and subjects received a high-fat mixed meal (2.6 MJ, 61 energy% fat) containing [U-(13)C]-palmitate to label chylomicron-TAG.
  
  
  RESULTS
  Postprandial circulating TAG concentrations were significantly lower after dietary intervention in the LFHCCn-3 group compared to the HSFA group (DeltaiAUC -139+/-67 vs 167+/-70 micromol l(-1) min(-1), P=0.009), together with decreased concentrations of [U-(13)C]-labeled TAG, representing dietary FA. Fasting TAG clearance across forearm muscle was decreased on the HSFA diet, whereas no differences were observed in postprandial forearm muscle FA handling between diets.
  
  
  CONCLUSIONS
  Chronic manipulation of dietary fat quantity and quality did not affect forearm muscle FA handling in men with the MetS. Postprandial TAG concentrations decreased on the LFHCCn-3 diet, which could be (partly) explained by lower concentration of dietary FA in the circulation.
authors.affiliation: Department of Human Biology, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Centre, Maastricht, The Netherlands.
authors.forename: A M J
authors.initials: AM
authors.lastname: van Hees
authors.forename: W H M
authors.initials: WH
authors.lastname: Saris
authors.forename: G B
authors.initials: GB
authors.lastname: Hul
authors.forename: N C
authors.initials: NC
authors.lastname: Schaper
authors.forename: B E
authors.initials: BE
authors.lastname: Timmerman
authors.forename: J A
authors.initials: JA
authors.lastname: Lovegrove
authors.forename: H M
authors.initials: HM
authors.lastname: Roche
authors.forename: E E
authors.initials: EE
authors.lastname: Blaak
mesh_terms: D000328:Adult; D000368:Aged; D004041:Dietary Fats / Q000008:administration & dosage / Q000378:metabolism*; D005215:Fasting; D005227:Fatty Acids / Q000097:blood*; D005247:Feeding Behavior / Q000502:physiology*; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism*; D019518:Postprandial Period
chemical_list: D004041:Dietary Fats; D005227:Fatty Acids