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1 Institute of Biology and Medical Genetics, First Faculty of Medicine, Charles Uiversity in Prague, Prague, Czech Republic; Centre de Recherche, Centre Hospitalier de l, Montreal, Canada
2 Institute of Biology and Medical Genetics, First Faculty of Medicine, Charles Uiversity in Prague, Prague, Czech Republic; Centre de Recherche, Centre Hospitalier de l, Montreal, Canada; Department of Metabolism and Diabetes, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
3 Department of Metabolism and Diabetes, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
4 Institute of Biology and Medical Genetics, First Faculty of Medicine, Charles Uiversity in Prague, Prague, Czech Republic
5 Centre de Recherche, Centre Hospitalier de l, Montreal, Canada
* To whom correspondence should be addressed. E-mail: lsedo{at}lf1.cuni.cz.
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 high-sucrose (70% calories as sucrose) diets starting one week before breeding, throughout pregnancy, birth and until weaning of the offspring. After weaning, all male offspring were fed HSD until the age of 20 weeks, when detailed metabolic and morphometric profiles were ascertained. The early life exposure to a sucrose-rich diet resulted in distinct responses to long-time postnatal HSD feeding. Offspring of the sucrose-fed mothers displayed higher adiposity, 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 to 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.
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