AI Article Synopsis

  • - The research focused on the role of estrogen receptor alpha (ESR1) in male rats, specifically looking at how the absence of ESR1 affects metabolic functions in the liver.
  • - RNA-sequencing was used to analyze liver gene expression, revealing 618 genes that were significantly altered in male rats lacking ESR1 compared to normal rats.
  • - Pathway analyses suggested that these differentially expressed genes primarily influence carbohydrate and lipid metabolism, with further details provided in a related manuscript.

Article Abstract

Estrogens are traditionally considered to be female sex steroid hormones and most of the studies examining estrogen regulation of metabolic function in the liver have been conducted in females. However, the liver expresses high levels of estrogen receptor alpha (ESR1) in both males and females, which mediates the hepatic response to estrogens. In this data article, we investigated whether metabolic disorders in knockout () male rats were linked with loss of transcriptional regulation by ESR1 in liver. To identify the ESR1 regulated genes in the mutant liver, RNA-sequencing was performed on liver RNAs purified from young male rats. The raw data were analyzed using the CLC Genomics Workbench and high-quality RNA-sequencing reads were aligned to the genome. Transcriptome data obtained from liver RNAs were compared to that of wild type rats. Based on an absolute fold change of 2 with a -value ≤ 0.05, a total of 618 differentially expressed genes were identified in the male liver. Pathway analyses demonstrated that the majority of differentially expressed genes are regulators of carbohydrate and lipid metabolism in the liver. These differentially expressed genes and their potential roles were further examined in a companion manuscript, "Disruption of ESR1 alters the expression of genes regulating hepatic lipid and carbohydrate metabolism in male rats" (Khristi et al., 2018).

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6330359PMC
http://dx.doi.org/10.1016/j.dib.2018.12.089DOI Listing

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