GNAS gene is an important regulator of insulin secretory capacity in pancreatic β-cells

Gene. 2019 Oct 5:715:144028. doi: 10.1016/j.gene.2019.144028. Epub 2019 Jul 30.

Abstract

Background: Type 2 diabetes (T2D) is a complex polygenic disease with unclear mechanism. In an attempt to identify novel genes involved in β-cell function, we harness a bioinformatics method called Loss-of-function tool (LoFtool) gene score.

Methods: RNA-sequencing data from human islets were used to cross-reference genes within the 1st quartile of most intolerant LoFtool score with the 100th most expressed genes in human islets. Out of these genes, GNAS and EEF1A1 genes were selected for further investigation in diabetic islets, metabolic tissues along with their correlation with diabetic phenotypes. The influence of GNAS and EEF1A1 on insulin secretion and β-cell function were validated in INS-1 cells.

Results: A comparatively higher expression level of GNAS and EEF1A1 was observed in human islets than fat, liver and muscle tissues. Furthermore, diabetic islets displayed a reduced expression of GNAS, but not of EEF1A, compared to non-diabetic islets. The expression of GNAS was positively correlated with insulin secretory index, GLP1R, GIPR and inversely correlated with HbA1c. Diabetic human islets displayed a reduced cAMP generation and insulin secretory capacity in response to glucose. Moreover, siRNA silencing of GNAS in INS-1 cells reduced insulin secretion, insulin content, and cAMP production. In addition, the expression of Insulin, PDX1, and MAFA was significantly down-regulated in GNAS-silenced cells. However, cell viability and apoptosis rate were unaffected.

Conclusion: LoFtool is a powerful tool to identify genes associated with pancreatic islets dysfunction. GNAS is a crucial gene for the β-cell insulin secretory capacity.

Keywords: GNAS; Human pancreatic islets; INS-1 cells; Insulin secretion; RNA sequencing; siRNA silencing.

MeSH terms

  • Aged
  • Animals
  • Cell Line
  • Chromogranins / biosynthesis*
  • Chromogranins / genetics
  • Cyclic AMP / genetics
  • Cyclic AMP / metabolism
  • Female
  • GTP-Binding Protein alpha Subunits, Gs / biosynthesis*
  • GTP-Binding Protein alpha Subunits, Gs / genetics
  • Gene Expression Regulation*
  • Humans
  • Insulin Secretion*
  • Insulin-Secreting Cells / cytology
  • Insulin-Secreting Cells / metabolism*
  • Male
  • Middle Aged
  • Organ Specificity
  • Peptide Elongation Factor 1 / genetics
  • Peptide Elongation Factor 1 / metabolism
  • Rats

Substances

  • Chromogranins
  • EEF1A1 protein, human
  • EEF1A1 protein, rat
  • Peptide Elongation Factor 1
  • Cyclic AMP
  • GNAS protein, human
  • Gnas protein, rat
  • GTP-Binding Protein alpha Subunits, Gs