title: Delayed post-prandial lipid metabolism in subjects with intra-abdominal visceral fat accumulation.
abstract: BACKGROUND
  Individuals with obesity, in particular those with intra-abdominal visceral fat accumulation, are known to have various complications, such as hyperlipidaemia, impaired glucose tolerance, hyperinsulinaemia and hypertension, leading to the development of coronary heart disease. Post-prandial hyperlipidaemia has repeatedly been shown to be an independent risk factor for coronary heart disease. The aim of the present study was to investigate post-prandial lipoprotein metabolism in subjects with excessive visceral fat accumulation.
  
  
  METHODS
  Eighty-three patients (52 men, 31 women) [average age 48 +/- 14 years; mean body mass index (BMI) 25 +/- 5 kg m-2] were recruited to the study. Visceral (or subcutaneous) fat accumulation was analysed as areas of fat deposition by computerized tomography at the umbilicus level. After a 12-h overnight fast, oral vitamin A and a fatty meal (40 g m-2 fresh cream containing 50 000 units m-2 vitamin A) were administered to these subjects. The concentration of retinyl palmitate (RP) was measured by high-performance liquid chromatography.
  
  
  RESULTS
  The visceral fat area (V) was positively correlated with plasma triglyceride (TG) 0, 2, 4 and 6 h after fat loading and with plasma RP 0, 4 and 6 h after fat loading. The BMI did not show any correlation with plasma TG and RP at any point. The visceral fat area was positively correlated with the RP area under the curve (AUC) in the serum from the subjects [V vs. RP AUC: n = 83, r = 0.327, P = 0.013]. The BMI of the subjects did not show any correlation with the RP AUC (r = 0.021, P = 0.85).
  
  
  CONCLUSIONS
  These results suggest that post-prandial lipid metabolism is impaired in subjects with intra-abdominal visceral fat accumulation, irrespective of BMI, leading to the development and progression of coronary atherosclerosis.
authors.affiliation: Chiba University, Chiba 260-8670, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Taira
authors.forename: M
authors.initials: M
authors.lastname: Hikita
authors.forename: J
authors.initials: J
authors.lastname: Kobayashi
authors.forename: H
authors.initials: H
authors.lastname: Bujo
authors.forename: K
authors.initials: K
authors.lastname: Takahashi
authors.forename: S
authors.initials: S
authors.lastname: Murano
authors.forename: N
authors.initials: N
authors.lastname: Morisaki
authors.forename: Y
authors.initials: Y
authors.lastname: Saito
mesh_terms: D000005:Abdomen; D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D000368:Aged; D016588:Anticarcinogenic Agents / Q000008:administration & dosage; D001057:Apolipoproteins E / Q000235:genetics / Q000378:metabolism; D015992:Body Mass Index; D004041:Dietary Fats / Q000008:administration & dosage / Q000378:metabolism*; D004224:Diterpenes; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000188:drug therapy / Q000378:metabolism; D008071:Lipoprotein Lipase / Q000097:blood; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000378:metabolism*; D010641:Phenotype; D019518:Postprandial Period; D012044:Regression Analysis; D000084562:Retinyl Esters; D014280:Triglycerides / Q000097:blood; D014781:Viscera; D014801:Vitamin A / Q000008:administration & dosage / Q000031:analogs & derivatives
chemical_list: D016588:Anticarcinogenic Agents; D001057:Apolipoproteins E; D004041:Dietary Fats; D004224:Diterpenes; D000084562:Retinyl Esters; D014280:Triglycerides; D014801:Vitamin A; C014794:retinol palmitate; D008071:Lipoprotein Lipase