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This Article Full Text Full Text (PDF) All Versions of this Article: 292/5/E1318    most recent 00526.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Sedová, L. Articles by Krenová, D. Search for Related Content PubMed PubMed Citation Articles by Sedová, L. Articles by Krenová, D.

Sucrose feeding during pregnancy and lactation elicits distinct metabolic response in offspring of an inbred genetic model of metabolic syndrome

Lucie edová,^1,3 Ondej eda,^1,2,3 Ludmila Kazdová,² Blanka Chylíková,¹ Pavel Hamet,³ Johanne Tremblay,³ Vladimír Ken,¹ and Drahomíra Kenová¹

¹Institute of Biology and Medical Genetics of the First Faculty of Medicine of Charles University and the General Teaching Hospital; ²Department of Metabolism and Diabetes, Institute for Clinical and Experimental Medicine, Prague, Czech Republic; and ³Centre de Recherche, Centre Hospitalier de l'Universite de Montreal, Montreal, Quebec, Canada

Submitted 27 September 2006 ; accepted in final form 7 January 2007

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.

developmental plasticity; animal model; PD/Cub; maternal diet

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