title: Fat oxidation before and after a high fat load in the obese insulin-resistant state.
abstract: BACKGROUND
  Obesity may be associated with a lowered use of fat as a fuel, which may contribute to the enlarged adipose tissue stores.
  
  
  OBJECTIVE
  The aim of the present study was to study fatty acid use in the fasting state and in response to a high fat load in a large cohort of obese subjects (n = 701) and a lean reference group (n = 113).
  
  
  METHODS
  Subjects from eight European centers underwent a test meal challenge containing 95 en% fat [energy content 50% of estimated resting energy expenditure (EE)]. Fasting and postprandial fat oxidation and circulating metabolites and hormones were determined over a 3-h period.
  
  
  RESULTS
  Postprandial fat oxidation (as percent of postprandial EE, adjusted for fat mass, age, gender, center, and energy content of the meal) decreased with increasing body mass index (BMI) category (P < 0.01), an effect present only in those obese subjects with a relatively low fasting fat oxidation (below median, interaction BMI category x fasting fat oxidation, P < 0.001). Fasting fat oxidation increased with increasing BMI category (P < 0.001), which was normalized after adjustment for fat-free mass and fat mass. Furthermore, insulin resistance was positively associated with postprandial fat oxidation (P < 0.05) and negatively associated with fasting fat oxidation (expressed as percent of EE), independent of body composition.
  
  
  CONCLUSIONS
  The present data indicate an impaired capacity to regulate fat oxidation in the obese insulin-resistant state, which is hypothesized to play a role in the etiology of both obesity and insulin resistance.
authors.affiliation: Department of Human Biology, Nutrition Research Centre, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands. e.blaak@hb.unimaas.nl
authors.forename: Ellen E
authors.initials: EE
authors.lastname: Blaak
authors.forename: Gabby
authors.initials: G
authors.lastname: Hul
authors.forename: Camilla
authors.initials: C
authors.lastname: Verdich
authors.forename: Vladimir
authors.initials: V
authors.lastname: Stich
authors.forename: Alfredo
authors.initials: A
authors.lastname: Martinez
authors.forename: Martin
authors.initials: M
authors.lastname: Petersen
authors.forename: Edith F M
authors.initials: EF
authors.lastname: Feskens
authors.forename: Kishor
authors.initials: K
authors.lastname: Patel
authors.forename: Jean Michel
authors.initials: JM
authors.lastname: Oppert
authors.forename: Pierre
authors.initials: P
authors.lastname: Barbe
authors.forename: Søren
authors.initials: S
authors.lastname: Toubro
authors.forename: Ingalena
authors.initials: I
authors.lastname: Anderson
authors.forename: Jan
authors.initials: J
authors.lastname: Polak
authors.forename: Arne
authors.initials: A
authors.lastname: Astrup
authors.forename: Ian A
authors.initials: IA
authors.lastname: Macdonald
authors.forename: Dominique
authors.initials: D
authors.lastname: Langin
authors.forename: Claus
authors.initials: C
authors.lastname: Holst
authors.forename: Thorkild I
authors.initials: TI
authors.lastname: Sørensen
authors.forename: Wim H M
authors.initials: WH
authors.lastname: Saris
mesh_terms: D000328:Adult; D019540:Area Under Curve; D001823:Body Composition / Q000502:physiology; D015992:Body Mass Index; D001835:Body Weight; D004041:Dietary Fats / Q000378:metabolism* / Q000494:pharmacology*; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D020738:Leptin / Q000097:blood; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000378:metabolism*; D010084:Oxidation-Reduction; D012727:Sex Characteristics
chemical_list: D004041:Dietary Fats; D020738:Leptin; D007334:Insulin-Like Growth Factor I; D006854:Hydrocortisone