Maternal Fructose Intake Increases Liver H S Synthesis but Exarcebates its Fructose-Induced Decrease in Female Progeny.

Scope: Fructose intake from added sugars correlates with the epidemic rise in metabolic syndrome and cardiovascular diseases (CVD). However, consumption of beverages containing fructose is allowed during gestation. Homocysteine (Hcy) is a well-known risk factor for CVD while hydrogen sulfide (H S), a product of its metabolism, has been proved to exert opposite effects to Hcy.

Methods And Results: First, it is investigated whether maternal fructose intake produces subsequent changes in Hcy metabolism and H S synthesis of the progeny. Carbohydrates are supplied to pregnant rats in drinking water (10% wt/vol) throughout gestation. Adult female descendants from fructose-fed, control or glucose-fed mothers are studied. Females from fructose-fed mothers have elevated homocysteinemia, hepatic H S production, cystathionine γ-lyase (CSE) (the key enzyme in H S synthesis) expression and plasma H S, versus the other two groups. Second, it is studied how adult female progeny from control (C/F), fructose- (F/F), and glucose-fed (G/F) mothers responded to liquid fructose and compared them to the control group (C/C). Interestingly, hepatic CSE expression and H S synthesis are diminished by fructose intake, this effect being more pronounced in F/F females.

Conclusion: Maternal fructose intake produces a fetal programming that increases hepatic H S production and, in contrast, exacerbates its fructose-induced drop in female progeny.