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The fetal programming of dietary fructose and saturated fat on hepatic quercetin glucuronidation in rats
Author(s) -
Chen C-Y. Oliver,
Bryant Nyssa,
Blumberg Jeffrey,
Serra Aida
Publication year - 2012
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.26.1_supplement.124.1
Subject(s) - glucuronidation , medicine , endocrinology , fructose , offspring , chemistry , weaning , corn oil , in utero , lactation , quercetin , fetus , glucuronide , microsome , metabolite , in vitro , biology , pregnancy , biochemistry , antioxidant , genetics
Polyphenol metabolites generated by phase II enzymes in vivo are bioactive. However, data on the impact of diet and fetal programming on the activity of microsomal UDP‐glucuronosyltransferase (UGT) are limited. We examined the effect of parental exposure to a diet high in fructose and saturated fat (SFF) 1 mo before conception and during gestation and lactation on in vitro hepatic UGT activity toward quercetin (Q) in parent (F0) and offspring (F1) rats. The SFF diet included 9.9% coconut fat, 0.5% cholesterol, 30% fructose, and 30% glucose and the control diet (C) 11% corn oil and 60% glucose. After weaning, all offspring were fed C diet for 12 wk. UGT activity was determined with 30 μM Q and 12.5 μg protein in 100 μL after a 15‐min incubation at 37°C. There was a sex and diet interaction on production rate of 3’‐ (3’‐OH), 4’‐ (4’‐OH), 7‐Q‐glucuronide (7‐OH), and total Q glucuronide (TQG). In F0 females, the production rate of 3’‐OH and TQG was decreased by 29 and 35% by SFF as compared to C (P ≤0.05). SFF led to a 22% difference in 4’‐OH production rate between females and males of the F0. In F1, the production rate of 7‐OH in C females was 59% larger than C males, but not different in SFF rats. Thus, high dietary fructose and saturated fat may decrease UGT activity toward Q in female rats and in utero exposure to this diet may decrease UGT activity in female offspring, possibly via epigenetic mechanisms.