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

Abstract

Pregnancy is a known risk factor for cardiometabolic morbidity and mortality; therefore, consuming fructose-containing energy drinks during pregnancy may worsen these risks. However, the mechanisms through which acetate alleviates fructose-induced cardiometabolic disturbances in pregnancy remain unclear. This study aimed to investigate the role of sodium acetate in modulating fructose-induced cardiometabolic risks during pregnancy. Thirty-six female Wistar rats (120–150 g) were assigned to six groups (n = 6). Eighteen rats were made pregnant and eighteen remained non-pregnant. Each physiological category consisted of three groups: control (C), fructose (F), and fructose + acetate (FA). The FA group received 10% (w/v) fructose plus sodium acetate (200 mg/kg) in addition to distilled water. After three weeks of treatment, animals were anesthetized with ketamine (90 mg/kg) and xylazine (10 mg/kg). Blood samples and cardiac tissue homogenates were collected for biochemical analysis. Data were expressed as mean ± SEM, and statistical significance was accepted at p < 0.05. Compared with the control groups, fasting blood sugar (FBS), triglyceride–glucose (TyG) index, circulatory free fatty acids (FFA), uric acid (UA), malondialdehyde (MDA), and lactate dehydrogenase (LDH) levels were significantly elevated in fructose-treated pregnant and non-pregnant rats. Conversely, high-density lipoprotein cholesterol (HDL), pyruvate dehydrogenase (PDH), and cardiac aconitase activities were significantly reduced in both states compared with control, with reductions more pronounced in pregnant rats. Pregnancy further exacerbated fructose-induced alterations in UA, FFA, TG, HDL, and MDA. Sodium acetate supplementation effectively mitigated these cardiometabolic disturbances irrespective of gestational status. Sodium acetate restores mitochondrial oxidative capacity in pregnancy, making it a potential therapeutic agent for improving mitochondrial metabolic activity and preventing debilitating gestational cardiometabolic disorders