title: One day of mixed meal overfeeding reduces hepatic insulin sensitivity and increases VLDL particle but not VLDL-triglyceride secretion in overweight and obese men.
abstract: BACKGROUND
  The exact mechanisms responsible for increased plasma triglyceride (TG) concentration in obese people are unclear, and it is not known whether excess energy intake per se is involved in the pathophysiology of this abnormality.
  
  
  OBJECTIVE
  The purpose of our study was to examine how excess energy intake from a balanced diet for 1 day affects very-low-density lipoprotein (VLDL)-TG kinetics and its putative regulators hepatic insulin sensitivity and plasma free fatty acid availability.
  
  
  METHODS
  We used stable isotope-labeled tracer methods to evaluate glucose and lipid kinetics in 8 overweight and obese men (age, 38 ± 3 years; body mass index, 33.7 ± 1.7 kg/m(2); means ± SEM) on 2 occasions (randomized crossover design): once, the day after they consumed a balanced diet that provided an amount of energy that matched their energy expenditure, and another time, the day after they consumed a balanced diet that provided 30% excess calories. Eight healthy, lean men (34 ± 1 years; 22.5 ± 0.6 kg/m(2)) were studied under isocaloric conditions only to provide a reference for normal lipid kinetics.
  
  
  RESULTS
  VLDL-TG and VLDL-apolipoprotein B-100 (apoB-100) concentrations and secretion rates were significantly greater (P < .01) in overweight/obese compared with lean men. Hypercaloric, compared with isocaloric, feeding in overweight/obese men increased glucose rate of appearance in plasma (904 ± 21 vs 873 ± 26 μmol/min), the hepatic insulin resistance index (10.9 ± 2.2 vs 8.3 ± 1.8), and VLDL-apoB-100 concentration and secretion rate (1.91 ± 0.24 vs. 1.53 ± 0.13 nmol/min), whereas VLDL-apoB-100 plasma clearance rate, VLDL-TG secretion and plasma clearance rates, and free fatty acid rate of appearance in plasma were not affected by overfeeding.
  
  
  CONCLUSIONS
  One day of moderate overfeeding (30% excess energy intake) stimulates hepatic glucose and VLDL-apo B-100 secretion rates but has no effect on hepatic and adipose tissue fatty acid metabolism in overweight/obese men.
authors.affiliation: Washington University School of Medicine, St Louis, Missouri 63110, USA.
authors.forename: Gordon I
authors.initials: GI
authors.lastname: Smith
authors.forename: Faidon
authors.initials: F
authors.lastname: Magkos
authors.forename: Dominic N
authors.initials: DN
authors.lastname: Reeds
authors.forename: Adewole L
authors.initials: AL
authors.lastname: Okunade
authors.forename: Bruce W
authors.initials: BW
authors.lastname: Patterson
authors.forename: Bettina
authors.initials: B
authors.lastname: Mittendorfer
mesh_terms: D000328:Adult; D053299:Apolipoprotein B-100 / Q000378:metabolism; D018592:Cross-Over Studies; D002149:Energy Intake; D005230:Fatty Acids, Nonesterified / Q000097:blood; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008079:Lipoproteins, VLDL / Q000378:metabolism*; D008297:Male; D009765:Obesity / Q000378:metabolism*; D044343:Overnutrition / Q000378:metabolism*; D050177:Overweight / Q000378:metabolism*; D014280:Triglycerides / Q000378:metabolism*
chemical_list: D053299:Apolipoprotein B-100; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D008079:Lipoproteins, VLDL; D014280:Triglycerides; C030106:very low density lipoprotein triglyceride