Assessing the epigenetics effects on the expression of the Fabp3 promoter region of Zinc‐Transporter 7‐deficient mice

Abstract

Zinc is an essential trace mineral for life. Zinc transporter 7 (ZNT7) transports zinc from the cytosol to the Golgi to maintain cellular zinc homeostasis. Mice with null‐Znt7 gene expression exhibit low zinc status, low body weight, as well as alterations in glucose and triglyceride homeostasis leading to a reduction in fat storage in adipocytes, and subsequently an increase in fat accumulation in muscle. The increase in muscle‐triglycerides in the Znt7KO mice is accompanied by a surge in the expression of Fabp3. Fatty‐Acid binding proteins (FABPs) belong to a family of proteins involved in intracellular lipid transport and status, yet some functions remain unknown. Fabp3 is found to be abundantly expressed in the heart, but it can also be moderately detected in skeletal muscle. Altered Fabp3 expression has been linked to a higher risk of developing metabolic syndrome in humans, hence this area of research is promising as rates of obesity and obesity‐related diseases continue to rise. DNA methylation has been shown to regulate human Fabp3 mRNA expression. Therefore, we aim to discover the methylation status of the mouse Fabp3 gene in a zinc deficient state using Znt7KO mice and determine a relationship between cellular zinc deficiency and the increased lipid accumulation in muscle, a cause of insulin resistance in Znt7KO male mice. Our preliminary results indicate that the cellular zinc level‐related DNA demethylation mainly occur in the area surround the transcriptional start site of Fabp3.Support or Funding InformationUSDA/ARS 2032‐51000‐005‐00D