Maternal fructose consumption during pregnancy and lactation is associated with metabolic dysregulation in offspring. We tested the hypothesis that fish oil (FO) supplementation during pregnancy and lactation improves fructose-induced metabolic dysregulation in postpartum dams and offspring mice. We therefore aimed to determine the effects of FO supplementation on metabolic disruption in neonatal mice and dams induced by a maternal high-fructose diet (HFrD). The weight of the offspring of dams fed with HFrD on postnatal day 5 was significantly low, but this was reversed by adding FO to the maternal diet. Feeding dams with HFrD significantly increased plasma concentrations of triglycerides, uric acid, and total cholesterol, and decreased free fatty acid concentrations in offspring. Maternal supplementation with FO significantly suppressed HFrD-induced hypertriglyceridemia and hyperuricemia in the offspring. Maternal HFrD induced remarkable mRNA expression of the lipogenic genes Srebf1, Fasn, Acc1, Scd1, and Acly in the postpartum mouse liver without affecting hepatic and plasma lipid levels. Although expression levels of lipogenic genes were higher in the livers of postpartum dams than in those of nonmated mice, HFrD feeding increased the hepatic lipid accumulation in nonmated mice but not in postpartum dams. These findings suggest that although hepatic lipogenic activity is higher in postpartum dams than nonmated mice, the lipid consumption is enhanced in postpartum dams during pregnancy and lactation. Maternal FO supplementation obviously suppressed the expression of these lipogenic genes. These findings coincide with reduced plasma triglyceride concentrations in the offspring. Therefore, dietary FO apparently ameliorated maternal HFrD-induced dyslipidemia in offspring by suppressing maternal lipogenic gene expression and/or neonatal plasma levels of uric acid.

中文翻译：

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母体鱼油补充剂通过抑制产后小鼠肝脏中脂肪生成基因的表达改善新生小鼠的母体高果糖饮食诱导的血脂异常

母体在怀孕和哺乳期间摄入果糖与后代代谢失调有关。我们测试了以下假设：在怀孕和哺乳期间补充鱼油 (FO) 可改善产后母鼠和后代小鼠中果糖引起的代谢失调。因此，我们旨在确定补充 FO 对由母体高果糖饮食 (HFrD) 诱导的新生小鼠和大坝代谢紊乱的影响。在产后第 5 天喂食 HFrD 的水坝的后代体重明显偏低，但通过在母体饮食中添加 FO 可以逆转这种情况。用 HFrD 喂养大坝显着增加了甘油三酯、尿酸和总胆固醇的血浆浓度，并降低了后代的游离脂肪酸浓度。母体补充 FO 显着抑制子代 HFrD 诱导的高甘油三酯血症和高尿酸血症。母体 HFrD 诱导产后小鼠肝脏中脂肪生成基因 Srebf1、Fasn、Acc1、Scd1 和 Acly 的显着 mRNA 表达，而不影响肝脏和血浆脂质水平。尽管产后母鼠肝脏中脂肪生成基因的表达水平高于未交配小鼠，但喂食 HFrD 会增加未交配小鼠的肝脏脂质积累，但不会增加产后母鼠的肝脏脂质积累。这些发现表明，虽然产后母鼠的肝脏脂肪生成活性高于未交配的小鼠，但产后母鼠在怀孕和哺乳期间的脂质消耗增加。母体FO补充剂明显抑制了这些脂肪生成基因的表达。这些发现与后代血浆甘油三酯浓度降低相吻合。因此，饮食 FO 通过抑制母体脂肪生成基因表达和/或新生儿血浆尿酸水平，明显改善了母体 HFrD 诱导的后代血脂异常。