title: Serum lipids, plant sterols, and cholesterol kinetic responses to plant sterol supplementation in phytosterolemia heterozygotes and control individuals.
abstract: BACKGROUND
  Plant sterol (PS) supplementation is increasingly accepted as a dietary strategy to lower plasma cholesterol concentrations. However, information is scarce about the effect of increased PS intake in potentially vulnerable groups, such as phytosterolemia heterozygotes (HET).
  
  
  OBJECTIVE
  This study assessed the responsiveness of circulating PS and lipid concentrations and cholesterol kinetics (absorption and synthesis) to daily PS supplementation in HET (ABCG8 S107X mutation) compared with a healthy control cohort.
  
  
  METHODS
  A double-blind, randomized, crossover, placebo-controlled study was conducted in 10 HET and 15 control subjects. The participants had a mean (±SEM) age of 34 ± 2 y and a BMI (in kg/m²) of 29.9 ± 1.1 and consumed ∼1.6 g PS or placebo capsules daily with supper for 4 wk. Cholesterol absorption and synthesis were assessed by using [¹³C]cholesterol and deuterium oxide, respectively.
  
  
  RESULTS
  Plasma LDL-cholesterol concentrations decreased (P = 0.006) in both groups after PS supplementation (HET: 2.73 ± 0.19 mmol/L; control: 3.11 ± 0.19 mmol/L) compared with placebo (HET: 3.12 ± 0.20 mmol/L; control: 3.50 ± 0.21 mmol/L), whereas PS concentrations (campesterol+β-sitosterol) increased (P = 0.03) in both groups after PS supplementation (HET: 39.72 ± 6.05 μmol/L; control: 24.03 ± 1.65 μmol/L) compared with placebo (HET: 27.32 ± 3.80 μmol/L; control: 21.12 ± 2.05 μmol/L). Cholesterol absorption efficiency decreased (P = 0.010) by ∼22% and ∼17% and synthesis rates increased (P = 0.040) by ∼20% and ∼24% in the HET and control groups, respectively, in response to PS consumption compared with placebo.
  
  
  CONCLUSIONS
  These data suggest that heterozygosity for the ABCG8 S107X mutation does not influence the action of dietary PS on circulating cholesterol concentrations but may affect sterol absorption.
authors.affiliation: Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Canada.
authors.forename: Semone B
authors.initials: SB
authors.lastname: Myrie
authors.forename: David
authors.initials: D
authors.lastname: Mymin
authors.forename: Barbara
authors.initials: B
authors.lastname: Triggs-Raine
authors.forename: Peter J H
authors.initials: PJ
authors.lastname: Jones
mesh_terms: D000071019:ATP Binding Cassette Transporter, Subfamily G, Member 8; D018528:ATP-Binding Cassette Transporters / Q000737:chemistry / Q000235:genetics*; D000293:Adolescent; D000328:Adult; D000368:Aged; D019943:Amino Acid Substitution; D002784:Cholesterol / Q000096:biosynthesis / Q000097:blood / Q000378:metabolism*; D015331:Cohort Studies; D018592:Cross-Over Studies; D019587:Dietary Supplements; D004311:Double-Blind Method; D005260:Female; D006579:Heterozygote; D006801:Humans; D006937:Hypercholesterolemia / Q000178:diet therapy* / Q000209:etiology / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D007408:Intestinal Absorption; D007410:Intestinal Diseases / Q000178:diet therapy* / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D007700:Kinetics; D008052:Lipid Metabolism, Inborn Errors / Q000178:diet therapy* / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D050505:Mutant Proteins / Q000737:chemistry / Q000235:genetics; D010840:Phytosterols / Q000009:adverse effects / Q000097:blood / Q000235:genetics / Q000378:metabolism / Q000627:therapeutic use*; D055815:Young Adult
chemical_list: C416946:ABCG8 protein, human; D000071019:ATP Binding Cassette Transporter, Subfamily G, Member 8; D018528:ATP-Binding Cassette Transporters; D008055:Lipids; D050505:Mutant Proteins; D010840:Phytosterols; D002784:Cholesterol