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Offspring from mothers fed a ‘junk food’ diet in pregnancy and lactation exhibit exacerbated adiposity that is more pronounced in females

机译:母亲的后代在怀孕和哺乳期间以垃圾食品饮食喂养后肥胖加剧而雌性则更为明显

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摘要

We have shown previously that a maternal junk food diet during pregnancy and lactation plays a role in predisposing offspring to obesity. Here we show that rat offspring born to mothers fed the same junk food diet rich in fat, sugar and salt develop exacerbated adiposity accompanied by raised circulating glucose, insulin, triglyceride and/or cholesterol by the end of adolescence (10 weeks postpartum) compared with offspring also given free access to junk food from weaning but whose mothers were exclusively fed a balanced chow diet in pregnancy and lactation. Results also showed that offspring from mothers fed the junk food diet in pregnancy and lactation, and which were then switched to a balanced chow diet from weaning, exhibited increased perirenal fat pad mass relative to body weight and adipocyte hypertrophy compared with offspring which were never exposed to the junk food diet. This study shows that the increased adiposity was more enhanced in female than male offspring and gene expression analyses showed raised insulin-like growth factor-1 (IGF-1), insulin receptor substrate (IRS)-1, vascular endothelial growth factor (VEGF)-A, peroxisome proliferator-activated receptor-γ (PPARγ), leptin, adiponectin, adipsin, lipoprotein lipase (LPL), Glut 1, Glut 3, but not Glut 4 mRNA expression in females fed the junk food diet throughout the study compared with females never given access to junk food. Changes in gene expression were not as marked in male offspring with only IRS-1, VEGF-A, Glut 4 and LPL being up-regulated in those fed the junk food diet throughout the study compared with males never given access to junk food. This study therefore shows that a maternal junk food diet promotes adiposity in offspring and the earlier onset of hyperglycemia, hyperinsulinemia and/or hyperlipidemia. Male and female offspring also display a different metabolic, cellular and molecular response to junk-food-diet-induced adiposity.
机译:以前我们已经表明,孕妇在怀孕和哺乳期间的垃圾食品饮食在使后代肥胖的过程中起着一定的作用。在这里,我们显示,与青春期结束时(产后10周)相比,喂食富含脂肪,糖和盐的垃圾食品的母亲所生的大鼠后代会加剧肥胖,并伴有循环葡萄糖,胰岛素,甘油三酸酯和/或胆固醇升高。后代还可以从断奶中免费获得垃圾食品,但其母亲在怀孕和哺乳期仅接受均衡的食物。结果还显示,母亲的后代在妊娠和哺乳期间以垃圾食品为食,然后从断奶改为平衡的日常饮食,与从未接触过的后代相比,相对于体重和脂肪细胞肥大,肾周脂肪垫质量增加。要吃垃圾食品。这项研究表明雌性增加的肥胖症比雄性后代更加加强,基因表达分析显示胰岛素样生长因子-1(IGF-1),胰岛素受体底物(IRS)-1,血管内皮生长因子(VEGF)升高在整个研究中,饲喂垃圾食品的女性中的-A,过氧化物酶体增殖物激活受体-γ(PPARγ),瘦素,脂联素,脂肪酶,脂蛋白脂肪酶(LPL),谷胱甘肽1,谷氨酸3,但不是谷胱甘肽4 mRNA表达与女性从未获得过垃圾食品。在整个研究过程中,饲喂垃圾食品的男性中,只有IRS-1,VEGF-A,Glut 4和LPL的表达上调,而雄性后代中的基因表达变化并不明显,而从未获得垃圾食品的男性中,IRS-1,VEGF-A,Glut 4和LPL的表达却没有上调。因此,这项研究表明,母亲的垃圾食品饮食可以促进后代的肥胖,并促进高血糖,高胰岛素血症和/或高脂血症的早发。男性和女性后代对垃圾食品饮食诱发的肥胖也表现出不同的代谢,细胞和分子反应。

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