Sedová Lucie, Seda Ondrej, Kazdová Ludmila, Chylíková Blanka, Hamet Pavel, Tremblay Johanne, Kren Vladimír, Krenová Drahomíra
Institute of Biology and Medical Genetics of the First Faculty of Medicine of Charles University and the General Teaching Hospital,Prague, Czech Republic.
Am J Physiol Endocrinol Metab. 2007 May;292(5):E1318-24. doi: 10.1152/ajpendo.00526.2006. Epub 2007 Jan 9.
The importance of early environment, including maternal diet during pregnancy, is suspected to play a major role in pathogenesis of metabolic syndrome and related conditions. One of the proposed mechanisms is a mismatch between the prenatal and postnatal environments, leading to misprogramming of the metabolic and signaling pathways of the developing fetus. We assessed whether the exposure to high-sucrose diet (HSD) alleviates the detrimental effects of sucrose feeding in later life (predictive adaptive hypothesis) in a highly inbred model of metabolic syndrome, the PD/Cub rat. Rat dams were continuously fed either standard or HSD (70% calories as sucrose) starting 1 wk before breeding, throughout pregnancy, at birth, and until weaning of the offspring. After weaning, all male offspring were fed HSD until the age of 20 wk, when detailed metabolic and morphometric profiles were ascertained. The early life exposure to a sucrose-rich diet resulted in distinct responses to longtime postnatal HSD feeding. Offspring of the sucrose-fed mothers displayed higher adiposity and substantial increases in triglyceride liver content together with unfavorable distribution of cholesterol into lipoprotein subfractions. On the other hand, their adiponectin concentrations were significantly higher, and insulin sensitivity of skeletal muscle was enhanced compared with the offspring of standard diet-fed mothers. Triglycerides, free fatty acids, overall glucose tolerance, and the insulin sensitivity of adipose tissue were comparable in both groups. In the genetically identical animals, maternal HSD feeding elicited a variety of subtle effects but did not lead to predictive adaptive protection from most HSD-induced metabolic derangements.
早期环境的重要性，包括孕期母亲的饮食，被怀疑在代谢综合征及相关病症的发病机制中起主要作用。一种提出的机制是产前和产后环境不匹配，导致发育中胎儿的代谢和信号通路编程错误。在一种高度近交的代谢综合征模型——PD/Cub大鼠中，我们评估了高蔗糖饮食（HSD）暴露是否能减轻后期生活中蔗糖喂养的有害影响（预测性适应假说）。从繁殖前1周开始，整个孕期、分娩时以及直到后代断奶，大鼠母鼠持续喂食标准饮食或HSD（70%热量来自蔗糖）。断奶后，所有雄性后代喂食HSD直至20周龄，此时确定详细的代谢和形态学特征。早期暴露于富含蔗糖的饮食导致对出生后长期HSD喂养有不同反应。喂食蔗糖的母亲的后代表现出更高的肥胖程度，肝脏甘油三酯含量大幅增加，同时胆固醇在脂蛋白亚组分中的分布不利。另一方面，与喂食标准饮食的母亲的后代相比，他们的脂联素浓度显著更高，骨骼肌的胰岛素敏感性增强。两组的甘油三酯、游离脂肪酸、总体葡萄糖耐量和脂肪组织的胰岛素敏感性相当。在基因相同的动物中，母鼠喂食HSD引发了多种细微影响，但并未导致对大多数HSD诱导的代谢紊乱的预测性适应性保护。
