Abstract
ObjectiveThis study aimed to evaluate the effects of microbe-derived antioxidant (MA) on high-fat diet (HFD)-induced hepatic lipid disorders in mother rats and offspring.MethodsA total of 36 female rats were randomly divided into three groups at the beginning of pregnancy: the control group (CG), HFD, and HFD with 2% MA. Mother rats were slaughtered at the first and 10th day of lactation (L1 and L10) and offspring were slaughtered at L10. The plasma and liver of mother rats, and liver of offspring were collected.ResultsThe results showed that MA reversed HFD-induced activities of inducible nitric oxide synthase (iNOS) and antioxidative enzymes in liver of mother rats and offspring. In addition, MA reduced HFD-induced lipid accumulation through decreasing the low-density lipoprotein cholesterol (LDLC) content in plasma of mother rats and improving hepatic fatty acid synthase (FAS) in mother rats and offspring. MA decreased HFD-induced hepatic alkaline phosphatase (AKP) activity in liver of mother rats and offspring. Furthermore, MA reduced HFD-activated nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasome in liver of mother rats and offspring.ConclusionsMA supplementation reversed HFD-induced hepatic oxidative stress, lipid accumulation, NLRP3 inflammasome, and function in mother rats and offspring, suggesting MA can be functional ingredients to improve maternal-fetal health.
Highlights
This study aimed to evaluate the effects of microbe-derived antioxidant (MA) on high-fat diet (HFD)-induced hepatic lipid disorders in mother rats and offspring
The results showed that MA reversed HFD-induced activities of inducible nitric oxide synthase and antioxidative enzymes in liver of mother rats and offspring
The present study showed that MA supplementation during pregnancy and lactation improved HFD-induced hepatic redox status and function, decreased low-density lipoprotein cholesterol (LDLC) content in plasma and fatty acid synthase (FAS) activity in liver, and inhibited NLRP3 inflammasome in mother rats and offspring, implying that MA is beneficial and promising to prevent chronic diseases or metabolic syndrome in offspring
Summary
Conclusions: MA supplementation reversed HFD-induced hepatic oxidative stress, lipid accumulation, NLRP3 inflammasome, and function in mother rats and offspring, suggesting MA can be functional ingredients to improve maternal-fetal health. Animal studies recently have shown that high-fat diet (HFD) during pregnancy and lactation increases hepatic oxidative stress, lipid accumulation, inflammatory cytokines, and activation of signaling pathways, predisposing offspring to the development of metabolic disorders such as insulin resistance and nonalcoholic fatty liver disease [3,4,5].
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