Sodium Acetate Attenuates Fructose-Induced Mitochondrial Dysfunction and Cardiometabolic Disorders in Pregnant Wistar...

Area of Science:

• Biochemistry
• Physiology
• Pharmacology

Background:

• Cardiometabolic disorder is a major cause of death, with mitochondrial dysfunction implicated in its development.
• The protective effects of acetate against fructose-induced cardiometabolic issues during pregnancy are not well understood.

Purpose of the Study:

• To investigate how acetate influences fructose-induced cardiometabolic risks in pregnant rats.
• To explore acetate's role in modulating mitochondrial function in the context of pregnancy-related metabolic disturbances.

Main Methods:

• Thirty-six female Wistar rats were divided into control, fructose, and fructose-acetate groups, with half made pregnant.
• Fructose and sodium acetate were administered for three weeks.
• Blood and tissue samples were analyzed for metabolic markers, oxidative stress indicators, and mitochondrial enzyme activities.

Main Results:

• Fructose increased fasting blood sugar, triglyceride-glucose index, free fatty acids, uric acid, malondialdehyde, and lactate dehydrogenase in both pregnant and non-pregnant rats.
• Acetate administration counteracted these fructose-induced changes.
• Pregnancy worsened fructose-induced metabolic alterations, but acetate treatment mitigated these effects, restoring mitochondrial enzyme activities like pyruvate dehydrogenase and cardiac aconitase.

Conclusions:

• Acetate effectively mitigates fructose-induced cardiometabolic disturbances, regardless of pregnancy status.
• Acetate administration helps restore mitochondrial oxidative capacity, indicating its potential as a therapeutic agent for gestational cardiac disorders.
• This study highlights acetate's role in improving mitochondrial metabolic activities in pregnancy.