(3)妊娠中母体低蛋白栄養が胎児胎内プログラミングに及ぼす影響とその発現メカニズム(<特集>第58回シンポジウム1「妊娠と栄養・代謝-妊娠中の適切な栄養管理をめざして-」)

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Objective: Previous reports showed that fetal programming with a dietary protein restriction in pregnant rats causes hypertension in offspring, and that there is a definite distinction between males and females in the incidence of hypertension in adulthood. Therefore, we hypothesized that ovarian dysfunction may make hypertension worse induced by fetal programming and thus impair endothelial function. The aim of this study is to reveal mechanism of hypertension induced by maternal low protein diet and influence of estrogen on fetal programming. In addition, influence of maternal low protein diet on pregnancy in offspring was investigate to make impact to the next generation clear. Method: Wistar rats were fed a diet containing either 18% (group C)or 9% (L) casein throughout pregnancy. <exp. 1> On day 18 or 19 of gestation, pregnancy was terminated and then uterine arteries were dissected to investigate endothelial function with wire myograph. <exp. 2> After birth, the pups were culled to six female pups per litter. Half of the offspring in both the C and R groups were ovariectomized at day 50 (C-Ox, L-Ox), and the other half underwent a sham operation (C-Oi, L-Oi). Blood pressure was measured by tailcuff plethysmography at days 50, 75, 125, and 175. Between d 175 and 185, the mesenteric arteries were dissected and their vascular function was investigated with a wire myograph. In addition, the heart was dissected to investigate coronary fibrosis. <exp. 3> Offspring was mated from d70 to 125 and then litter size, fetal weight, and placental weight were measured on 19 or 20 day of gestation. Results: <exp. 1> The vasorelaxation to VEGF was significantly blunted by maternal low protein diet. <exp. 2> Birth weight was not significantly different between C and R. There was no significant difference between the groups in systolic blood pressure on d50 or d75. On d125, L-Ox had significantly higher systolic blood pressure than C-Ox. On d175, blood pressure was higher in L than in C, regardless of the presence of ovaries. The responses to bradykinin were significantly attenuated in L-Ox. <exp. 3> Urinary protein in offspring was increased in L and fetal and placental weights in L were smaller than those in C. Conclusions: This study showed that a maternal low-protein diet during pregnancy induced hypertension in rat offspring without intrauterine growth restriction. In addition, ovariectomized rats developed hypertension earlier than sham-operated rats did. The maternal low-protein diet blunted the vasorelaxation to bradykinin in offspring, and ovariectomy made the attenuation worse. The results also suggested that estrogen is related to the gender difference in hypertension of fetal programming. Furthermore, it is likely that fetal programming induced intrauterine growth retardation in the next generation.
社団法人日本産科婦人科学会の論文
2006-09-01

(3)妊娠中母体低蛋白栄養が胎児胎内プログラミングに及ぼす影響とその発現メカニズム(<特集>第58回シンポジウム1「妊娠と栄養・代謝-妊娠中の適切な栄養管理をめざして-」)

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