title: Postprandial triglyceridemia and carotid atherosclerosis in middle-aged subjects.
abstract: OBJECTIVE
  It has been suggested that a postprandial accumulation of triglyceride-rich lipoproteins promotes the development of atherosclerosis. This study was designed to test the hypothesis that postprandial lipemia is independently associated with intima-media thickening of the extracranial carotid arteries.
  
  
  METHODS
  Forty-seven middle-aged, moderately hypercholesterolemic individuals were recruited for a 1-day study of the lipemic response to a standard high-fat test meal. The formula was fed at a dose of 65 g fat/m2 body surface area, after a 14-hour fast, and blood was obtained for triglyceride analysis hourly for 8 hours. A baseline lipid profile was obtained. Each subject underwent a carotid ultrasound examination. The extent of alimentary lipemia (peak triglyceride response) was correlated with the carotid artery wall thickness as measured by B-mode ultrasound.
  
  
  RESULTS
  Univariate analyses indicated an inverse correlation between peak triglyceride response and high density lipoprotein cholesterol concentration and a direct correlation with male sex, baseline triglyceride concentration, background fat intake, and waist-to-hip ratio. Of these, the only variable that showed a univariate correlation with B-mode score was peak triglyceride response. Age and cigarette smoking were also correlated with B-mode score in univariate analyses. The correlation coefficient (r = 0.52) between peak triglyceride response to a fat-rich meal and B-mode score was significant (p less than 0.002) and remained so in multivariate analysis. Forward-selection stepwise regression resulted in the inclusion of only peak triglyceride response (p = 0.001) and smoking history (p = 0.005) as important predictors of carotid wall thickness in a linear model.
  
  
  CONCLUSIONS
  The association between lipemic response and carotid wall thickness suggests that prolonged exposure of arterial wall cells to triglyceride-rich chylomicron remnants enhances the atherogenic process.
authors.affiliation: Department of Medicine, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, N.C. 27157-1047.
authors.forename: J E
authors.initials: JE
authors.lastname: Ryu
authors.forename: G
authors.initials: G
authors.lastname: Howard
authors.forename: T E
authors.initials: TE
authors.lastname: Craven
authors.forename: M G
authors.initials: MG
authors.lastname: Bond
authors.forename: A P
authors.initials: AP
authors.lastname: Hagaman
authors.forename: J R
authors.initials: JR
authors.lastname: Crouse
mesh_terms: D002339:Carotid Arteries / Q000000981:diagnostic imaging; D002340:Carotid Artery Diseases / Q000097:blood* / Q000000981:diagnostic imaging; D002784:Cholesterol / Q000097:blood; D004435:Eating; D005260:Female; D006801:Humans; D002537:Intracranial Arteriosclerosis / Q000097:blood* / Q000000981:diagnostic imaging; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D012727:Sex Characteristics; D014280:Triglycerides / Q000097:blood*; D014463:Ultrasonography
chemical_list: D008055:Lipids; D014280:Triglycerides; D002784:Cholesterol