Maternal Fructose Intake Induces Insulin Resistance and Oxidative Stress in Male, but Not Female, Offspring
Objective. 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% wt/vol) throughout gestation produce...
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Language: | English |
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Wiley
2015-01-01
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Series: | Journal of Nutrition and Metabolism |
Online Access: | http://dx.doi.org/10.1155/2015/158091 |
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author | Lourdes Rodríguez Paola Otero María I. Panadero Silvia Rodrigo Juan J. Álvarez-Millán Carlos Bocos |
author_facet | Lourdes Rodríguez Paola Otero María I. Panadero Silvia Rodrigo Juan J. Álvarez-Millán Carlos Bocos |
author_sort | Lourdes Rodríguez |
collection | DOAJ |
description | Objective. 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% wt/vol) throughout gestation produces an impaired fetal leptin signalling. Therefore, we have investigated whether maternal fructose intake produces subsequent changes in their progeny. Methods. Blood samples from fed and 24 h fasted female and male 90-day-old rats born from fructose-fed, glucose-fed, or control mothers were used. Results. After fasting, HOMA-IR and ISI (estimates of insulin sensitivity) were worse in male descendents from fructose-fed mothers in comparison to the other two groups, and these findings were also accompanied by a higher leptinemia. Interestingly, plasma AOPP and uricemia (oxidative stress markers) were augmented in male rats from fructose-fed mothers compared to the animals from control or glucose-fed mothers. In contrast, female rats did not show any differences in leptinemia between the three groups. Further, insulin sensitivity was significantly improved in fasted female rats from carbohydrate-fed mothers. In addition, plasma AOPP levels tended to be diminished in female rats from carbohydrate-fed mothers. Conclusion. Maternal fructose intake induces insulin resistance, hyperleptinemia, and plasma oxidative stress in male, but not female, progeny. |
format | Article |
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institution | Kabale University |
issn | 2090-0724 2090-0732 |
language | English |
publishDate | 2015-01-01 |
publisher | Wiley |
record_format | Article |
series | Journal of Nutrition and Metabolism |
spelling | doaj-art-5cfccba3b0a24951b6b83a2847bec8512025-02-03T06:15:12ZengWileyJournal of Nutrition and Metabolism2090-07242090-07322015-01-01201510.1155/2015/158091158091Maternal Fructose Intake Induces Insulin Resistance and Oxidative Stress in Male, but Not Female, OffspringLourdes Rodríguez0Paola Otero1María I. Panadero2Silvia Rodrigo3Juan J. Álvarez-Millán4Carlos Bocos5Facultad de Farmacia, Universidad CEU San Pablo, Urbanización Montepríncipe, Boadilla del Monte, 28668 Madrid, SpainFacultad de Farmacia, Universidad CEU San Pablo, Urbanización Montepríncipe, Boadilla del Monte, 28668 Madrid, SpainFacultad de Farmacia, Universidad CEU San Pablo, Urbanización Montepríncipe, Boadilla del Monte, 28668 Madrid, SpainFacultad de Farmacia, Universidad CEU San Pablo, Urbanización Montepríncipe, Boadilla del Monte, 28668 Madrid, SpainFacultad de Farmacia, Universidad CEU San Pablo, Urbanización Montepríncipe, Boadilla del Monte, 28668 Madrid, SpainFacultad de Farmacia, Universidad CEU San Pablo, Urbanización Montepríncipe, Boadilla del Monte, 28668 Madrid, SpainObjective. 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% wt/vol) throughout gestation produces an impaired fetal leptin signalling. Therefore, we have investigated whether maternal fructose intake produces subsequent changes in their progeny. Methods. Blood samples from fed and 24 h fasted female and male 90-day-old rats born from fructose-fed, glucose-fed, or control mothers were used. Results. After fasting, HOMA-IR and ISI (estimates of insulin sensitivity) were worse in male descendents from fructose-fed mothers in comparison to the other two groups, and these findings were also accompanied by a higher leptinemia. Interestingly, plasma AOPP and uricemia (oxidative stress markers) were augmented in male rats from fructose-fed mothers compared to the animals from control or glucose-fed mothers. In contrast, female rats did not show any differences in leptinemia between the three groups. Further, insulin sensitivity was significantly improved in fasted female rats from carbohydrate-fed mothers. In addition, plasma AOPP levels tended to be diminished in female rats from carbohydrate-fed mothers. Conclusion. Maternal fructose intake induces insulin resistance, hyperleptinemia, and plasma oxidative stress in male, but not female, progeny.http://dx.doi.org/10.1155/2015/158091 |
spellingShingle | Lourdes Rodríguez Paola Otero María I. Panadero Silvia Rodrigo Juan J. Álvarez-Millán Carlos Bocos Maternal Fructose Intake Induces Insulin Resistance and Oxidative Stress in Male, but Not Female, Offspring Journal of Nutrition and Metabolism |
title | Maternal Fructose Intake Induces Insulin Resistance and Oxidative Stress in Male, but Not Female, Offspring |
title_full | Maternal Fructose Intake Induces Insulin Resistance and Oxidative Stress in Male, but Not Female, Offspring |
title_fullStr | Maternal Fructose Intake Induces Insulin Resistance and Oxidative Stress in Male, but Not Female, Offspring |
title_full_unstemmed | Maternal Fructose Intake Induces Insulin Resistance and Oxidative Stress in Male, but Not Female, Offspring |
title_short | Maternal Fructose Intake Induces Insulin Resistance and Oxidative Stress in Male, but Not Female, Offspring |
title_sort | maternal fructose intake induces insulin resistance and oxidative stress in male but not female offspring |
url | http://dx.doi.org/10.1155/2015/158091 |
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