Abstract

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.

Highlights

  • In the last few decades, obesity, metabolic syndrome, and diabetes have escalated to epidemic proportions in many countries worldwide

  • homeostasis model assessment of insulin resistance (HOMA-IR) and insulin sensitivity index (ISI) were worse in male descendents from fructose-fed mothers in comparison to the other two groups, and these findings were accompanied by a higher leptinemia

  • Estimates of insulin resistance were calculated as previously described [15, 25] by determination of the following indexes from the 24 h fasting plasma glucose and insulin values: homeostasis model assessment of insulin resistance (HOMA-IR) and insulin sensitivity index (ISI)

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Summary

Objective

Fructose intake from added sugars correlates with the epidemic rise in metabolic syndrome and cardiovascular diseases. We have investigated whether maternal fructose intake produces subsequent changes in their progeny. Blood samples from fed and 24 h fasted female and male 90day-old rats born from fructose-fed, glucose-fed, or control mothers were used. 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 accompanied by a higher leptinemia. 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. Insulin sensitivity was significantly improved in fasted female rats from carbohydrate-fed mothers. Plasma AOPP levels tended to be diminished in female rats from carbohydrate-fed mothers. Maternal fructose intake induces insulin resistance, hyperleptinemia, and plasma oxidative stress in male, but not female, progeny

Introduction
Material and Methods
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