title: Adequate Intake levels of choline are sufficient for preventing elevations in serum markers of liver dysfunction in Mexican American men but are not optimal for minimizing plasma total homocysteine increases after a methionine load.
abstract: BACKGROUND
  An adequate intake of 550 mg choline/d was established for the prevention of liver dysfunction in men, as assessed by measuring serum alanine aminotransferase concentrations.
  
  
  OBJECTIVE
  This controlled feeding study investigated the influence of choline intakes ranging from 300 to 2200 mg/d on biomarkers of choline status. The effect of the methylenetetrahydrofolate reductase (MTHFR) C677T genotype on choline status was also examined.
  
  
  METHODS
  Mexican American men (n = 60) with different MTHFR C677T genotypes (29 677TT, 31 677CC) consumed a diet providing 300 mg choline/d plus supplemental choline intakes of 0, 250, 800, or 1900 mg/d for total choline intakes of 300, 550, 1100, or 2200 mg/d, respectively, for 12 wk; 400 mug/d as dietary folate equivalents and 173 mg betaine/d were consumed throughout the study.
  
  
  RESULTS
  Choline intake affected the response of plasma free choline and betaine (time x choline, P < 0.001); the highest concentrations were observed in the 2200 mg/d group. Phosphatidylcholine (P = 0.026) and total cholesterol (P = 0.002) were also influenced by choline intake; diminished concentrations were observed in the 300 mg/d group. Phosphatidylcholine was modified by MTHFR genotype (P = 0.035; 677TT < 677CC). After a methionine load (100 mg/kg body wt), choline intakes of 1100 and 2200 mg/d attenuated (P = 0.016) the rise in plasma homocysteine, as did the MTHFR 677TT genotype (P < 0.001). Serum alanine aminotransferase was not influenced by the choline intakes administered in this study.
  
  
  CONCLUSIONS
  These data suggest that 550 mg choline/d is sufficient for preventing elevations in serum markers of liver dysfunction in this population under the conditions of this study; higher intakes may be needed to optimize other endpoints.
authors.affiliation: Department of Human Nutrition, Cal Poly Pomona, Pomona, CA, USA.
authors.forename: Kristin
authors.initials: K
authors.lastname: Veenema
authors.forename: Claudia
authors.initials: C
authors.lastname: Solis
authors.forename: Rui
authors.initials: R
authors.lastname: Li
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Charles V
authors.initials: CV
authors.lastname: Maletz
authors.forename: Christian M
authors.initials: CM
authors.lastname: Abratte
authors.forename: Marie A
authors.initials: MA
authors.lastname: Caudill
mesh_terms: D000293:Adolescent; D000328:Adult; D001622:Betaine / Q000097:blood; D002794:Choline / Q000008:administration & dosage / Q000097:blood / Q000378:metabolism* / Q000652:urine; D005838:Genotype; D006630:Hispanic or Latino; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D008297:Male; D008715:Methionine / Q000378:metabolism* / Q000494:pharmacology; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000235:genetics*; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D012016:Reference Values
chemical_list: D006710:Homocysteine; D001622:Betaine; D008715:Methionine; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D002794:Choline
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