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Choline intakes at AI levels are sufficient in preventing liver dysfunction in Mexican American men but are not optimal in minimizing plasma total homocysteine increases after a methionine load
Author(s) -
Caudill Marie A,
Veenema Kristin,
Solis Claudia,
Wang Wei,
Li Rui,
Maletz Charles
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.296.3
Subject(s) - choline , methionine , betaine , homocysteine , medicine , endocrinology , phosphatidylcholine , methylenetetrahydrofolate reductase , hyperhomocysteinemia , chemistry , population , dietary reference intake , biochemistry , phospholipid , amino acid , genotype , nutrient , environmental health , organic chemistry , membrane , gene
This controlled feeding study investigated the influence of choline intake ranging from 300 to 2200mg/d on biomarkers of choline status. Mexican American men (n=60) differing in methylenetetrahydrofolate reductase (MTHFR) C677T genotype (29 677TT, 31 677CC) consumed a diet providing 300mg/d choline plus supplemental choline intakes of 0, 250, 800 or 1900 mg/d for total choline intakes of 300, 550 (choline AI), 1100 or 2200mg/d, respectively for 12‐wk; 400mcg/d as dietary folate equivalents and 173mg/d betaine were consumed throughout the study. Plasma choline and betaine increased (P<0.05) in response to 550, 1100 and 2200mg/d choline (2200>1100=550) whereas no change was observed on the 300mg/d group. Plasma phosphatidylcholine declined (P<0.05) in response to 300mg/d possibly due to declining folate status; no changes were observed in the other choline intake groups. After a methionine load, choline intakes of 1100 and 2200 mg/d groups attenuated (P<0.006) the rise in plasma tHcy relative to the 300 and 550 mg/d groups. No changes in plasma ALT or AST concentrations were detected regardless of choline intake. These data suggest that 550 mg/d choline is sufficient to prevent liver dysfunction in this population; higher intakes are needed to optimize other measured end‐points. Supported by NIH Grant #S06GM053933.