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FOXN3 Regulates Hepatic Glucose Utilization.

Santhosh Karanth1, Erin K Zinkhan2, Jonathon T Hill3

  • 1University of Utah Molecular Medicine Program, University of Utah School of Medicine, Salt Lake City, UT 84112, USA; Division of Endocrinology, Metabolism and Diabetes, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, UT 84112, USA.

Cell Reports
|June 14, 2016
PubMed
Summary
This summary is machine-generated.

A specific gene variant (rs8004664) increases fasting blood glucose by elevating FOXN3 expression in the liver. This elevated FOXN3 disrupts glucose metabolism regulation, impacting MYC levels and contributing to higher blood sugar.

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Area of Science:

  • Genetics
  • Metabolism
  • Molecular Biology

Background:

  • A single nucleotide polymorphism (SNP), rs8004664, located in the first intron of the FOXN3 gene, has been linked to variations in human fasting blood glucose levels.
  • Individuals carrying the risk allele for this SNP exhibit increased hepatic expression of FOXN3, a transcriptional repressor.

Purpose of the Study:

  • To investigate the functional role of FOXN3 in regulating fasting blood glucose.
  • To elucidate the molecular mechanisms by which the rs8004664 SNP influences glucose homeostasis.

Main Methods:

  • Comparative analysis of FOXN3 expression in rat, zebrafish, and human hepatoma cells during fasting.
  • Transgenic overexpression studies in zebrafish to assess the impact of FOXN3 on gluconeogenesis and glycolysis.
  • Investigation of the interaction between FOXN3, MYC, and glucose metabolism-related genes.

Main Results:

  • FOXN3 expression is downregulated during fasting in various species, a process mimicked in human cells.
  • Overexpression of FOXN3 in zebrafish leads to increased gluconeogenic gene expression, elevated glucose levels, and decreased glycolytic gene expression.
  • Hepatic FOXN3 overexpression suppresses MYC expression, and carriers of the rs8004664 risk allele show reduced MYC transcript levels.

Conclusions:

  • The rs8004664 risk allele promotes excessive FOXN3 expression during fasting.
  • FOXN3 acts as a regulator of fasting blood glucose, potentially through its interaction with the MYC pathway and modulation of glucose metabolic gene expression.