Maternal Fructose Intake Increases Liver H₂ S Synthesis but Exarcebates its Fructose-Induced Decrease in Female...

Area of Science:

• Biochemistry
• Cardiovascular Science
• Developmental Biology

Background:

• Added sugar fructose intake is linked to metabolic syndrome and cardiovascular diseases (CVD).
• Homocysteine (Hcy) is a CVD risk factor, while hydrogen sulfide (H₂S) has protective effects.
• Fructose consumption is permitted during pregnancy, raising concerns about fetal programming.

Purpose of the Study:

• To investigate the effects of maternal fructose consumption on progeny's homocysteine metabolism and hydrogen sulfide synthesis.
• To determine how fructose exposure in utero influences the response to fructose in adulthood.

Main Methods:

• Pregnant rats received 10% fructose in drinking water throughout gestation.
• Adult female offspring from fructose-fed, control, or glucose-fed mothers were studied.
• Assessed homocysteine levels, hepatic H₂S production, cystathionine γ-lyase (CSE) expression, and plasma H₂S.

Main Results:

• Maternal fructose intake led to elevated homocysteinemia and increased hepatic H₂S production, CSE expression, and plasma H₂S in female offspring.
• Adult female offspring exposed to fructose in utero showed diminished hepatic CSE expression and H₂S synthesis upon subsequent fructose consumption.
• This fructose-induced reduction in H₂S synthesis was more pronounced in offspring of fructose-fed mothers.

Conclusions:

• Maternal fructose intake establishes fetal programming that elevates hepatic H₂S production in female progeny.
• This programming paradoxically exacerbates the suppressive effect of fructose on H₂S synthesis in adulthood.