Fructose only in pregnancy provokes hyperinsulinemia, hypoadiponectinemia and impaired insulin signaling in adult male, but not female, progeny.

dc.centroUniversidad San Pablo-CEU
dc.contributor.authorRodríguez, Lourdes
dc.contributor.authorBocos de Prada, Carlos
dc.contributor.authorPanadero Antón, María Isabel
dc.date2016
dc.date.accessioned2021-08-10T04:00:12Z
dc.date.available2021-08-10T04:00:12Z
dc.date.issued2016-08-10
dc.descriptionEn: European Journal of Nutrition. 2016. vol. 55 : 665-674 p. e-ISSN 1436-6215
dc.description.abstractPurpose Fructose intake from added sugars correlates with the epidemic rise in metabolic syndrome and cardiovascular diseases. However, consumption of beverages containing fructose is allowed during gestation. Recently, we found that an intake of fructose (10% 5 wt/vol) throughout gestation produces impaired fetal leptin signaling and hepatic steatosis. Therefore, we have investigated whether fructose intake during pregnancy produces subsequent changes in the progeny, when adult. 8 Methods Fed 261-day-old male and female descendants from fructose-fed, control or glucose9 fed mothers were used. Plasma was used to analyze glucose, insulin, leptin, and adiponectin. Hepatic expression of proteins related to insulin signaling was determined. Results Fructose intake throughout pregnancy did not produce alterations in the body weight of the progeny. Adult male progeny of fructose-fed mothers had elevated levels of insulin without a parallel increase in phosphorylation of protein kinase-B. However, they displayed an augmented serine phosphorylation of insulin receptor substrate-2, indicating reduced insulin signal transduction. In agreement, adiponectin levels, which have been positively related to insulin sensitivity, were lower in male descendants from fructose-fed mothers than in the other two groups. Furthermore, mRNA levels for insulin-responsive genes were not affected (phosphoenol pyruvate carboxykinase, glucose-6-phosphatase) or they were decreased (sterol response element-binding protein-1c) in the livers of male progeny from fructose-supplemented rats. On the contrary, adult female rats from fructose-fed mothers did not exhibit any of these disturbances. Conclusion Maternal fructose, but not glucose, intake confined to the prenatal stage provokes impaired insulin signal transduction, hyperinsulinemia, and hypoadiponectinemia in adult male, but not female, progeny.en-EN
dc.formatapplication/pdf
dc.identifier000000723160
dc.identifier.urihttp://hdl.handle.net/10637/12937
dc.language.isoen
dc.relationThis work was 11 supported by grants from the Instituto de Salud Carlos III-Subdirección General de Evaluación y 12 Fomento de la Investigación (PI-09/02192), European Community FEDER funds, SAF2013- 13 42982-R and from the Generalitat of Catalonia (2013SGR0066), as well as the Fundación 14 Universitaria San Pablo-CEU (PC 09/2012).en-EN
dc.rightsopen access
dc.rights.cchttps://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
dc.subjectFructose pregnancyen-EN
dc.subjectFetal programmingen-EN
dc.subjectMetabolic syndrome.en-EN
dc.titleFructose only in pregnancy provokes hyperinsulinemia, hypoadiponectinemia and impaired insulin signaling in adult male, but not female, progeny.
dc.typeArtículo
dspace.entity.typePublicationes
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relation.isAuthorOfPublicationadbfb759-8813-47dd-bf1d-3cc7a8eeb190
relation.isAuthorOfPublication.latestForDiscoveryaa357baa-d71a-431b-b1ce-6007bcceabf9

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