Maternal Fructose Intake Increases Liver H2S Synthesis but Exarcebates its Fructose‐Induced Decrease in Female Progeny

• Published in: Molecular nutrition & food research 2020-09, Vol.64 (18), p.n/a
• Main Authors: Fauste, Elena, Rodrigo, Silvia, Aguirre, Rodrigo, Donis, Cristina, Rodríguez, Lourdes, Álvarez‐Millán, Juan J., Panadero, María I., Otero, Paola, Bocos, Carlos
• Format: Article
• Language: English
• Subjects: Beverages; Carbohydrates; Cardiovascular diseases; Drinking water; Epidemics; Females; fetal programming; Fetuses; Fructose; Gestation; Glucose; Homocysteine; Hydrogen sulfide; Liver; Metabolic disorders; Metabolic syndrome; Metabolism; Offspring; oxidative stress; Progeny; Risk analysis; Risk factors; Sugar; Synthesis
• ISSN: 1613-4125; 1613-4133
• DOI: 10.1002/mnfr.202000628

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 (H2S), 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 H2S 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 H2S production, cystathionine γ‐lyase (CSE) (the key enzyme in H2S synthesis) expression and plasma H2S, 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 H2S 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 H2S production and, in contrast, exacerbates its fructose‐induced drop in female progeny. Fructose intake correlates with the epidemic rise in cardiovascular diseases (CVD). Hydrogen sulfide (H2S) is a protective factor against CVD. Maternal fructose produces in female progeny elevated hepatic H2S production and cystathionine γ‐lyase (CSE) expression. However, adult female progeny from control (C/F), fructose‐ (F/F), and glucose‐fed (G/F) mothers subjected to liquid fructose shows both CSE expression and H2S synthesis diminished.