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Original Research ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Endocrinol. | doi: 10.3389/fendo.2019.00735

Reduced expression of PLCXD3 associates with disruption of glucose sensing and insulin signalling in pancreatic β-cells

  • 1University of Sharjah, United Arab Emirates
  • 2Lund University, Sweden

Previous work has shown that reduced expression PLCXD3, a member of Phosphoinositide-specific phospholipases (PI-PLC) family, impaired insulin secretion with an unclear mechanism. In the current study, we aim to investigate the mechanism underlying this effect using human islets and in rat INS-1 (832/13) cells. Microarray and RNA sequencing data showed that PLCXD3 is among the highly expressed PI-PLCs in human islets and INS-1 (832/13) cells. Expression of PLCXD3 was reduced in human diabetic islets, correlated positively with Insulin, GLP1R expression and inversely with the donor’s body mass index (BMI) and glycated hemoglobin (HbA1c). Expression silencing of PLCXD3 in INS-1 (832/13) cells found to reduce glucose-stimulated insulin secretion (GSIS) and insulin content. In addition, the expression of Insulin, NEUROD1, GLUT2, GCK, INSRα, IRS2, and AKT were down-regulated. Cell viability and apoptosis rate were unaffected. In conclusion, our data suggest that low expression of PLCXD3 in pancreatic β-cells associates with down-regulation of the key insulin signalling and insulin biosynthesis genes as well as reduction in glucose sensing.

Keywords: phosphatidylinositol-specific phospholipase C X domain containing 3, PLCXD3, PI-PLC: Phosphatidylinositol-specific phospholipase C, T2D (type 2 diabetes), Pancreatic β-cells

Received: 12 Jul 2019; Accepted: 10 Oct 2019.

Copyright: © 2019 Aljaibeji, Mukhopadhyay, Mohammed, Dhaiban, hachim, Elemam, Sulaiman, Salehi and Taneera. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Jalal Taneera, University of Sharjah, Sharjah, United Arab Emirates, jtaneera@sharjah.ac.ae