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The Pancreatic INS-1E Beta Cells Activation of the TRPV4 Channel Increases the Release of Insulin in Response to Glucose Through Calcium- Dependent Processes| Abstract

Journal of Clinical Diabetes
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  • Review Article   
  • J Clin Diabetes 2023, Vol 7(3): 176

The Pancreatic INS-1E Beta Cells Activation of the TRPV4 Channel Increases the Release of Insulin in Response to Glucose Through Calcium- Dependent Processes

Harrty Burger*
Department of Clinical Diabetes, University of New Caledonia, New Caledonia
*Corresponding Author : Harrty Burger, Department of Clinical Diabetes, University of New Caledonia, New Caledonia, Email: burgerharrty80@gmail.com

Received Date: Apr 10, 2023 / Accepted Date: May 03, 2023 / Published Date: May 08, 2023

Abstract

Insulin secretion by pancreatic beta cells is a vital process for glucose regulation in the human body. The activation of the Transient Receptor Potential Vanilloid 4 (TRPV4) channel in these cells has recently been recognized as a significant contributor to insulin release. This study investigates the impact of TRPV4 channel activation on insulin secretion in response to glucose, with a particular focus on the involvement of calcium-dependent processes. Glucose-stimulated insulin secretion involves a cascade of events in pancreatic beta cells. Elevated blood glucose levels lead to glucose entry into beta cells and subsequent ATP production. ATP-sensitive potassium channels close as a result of increased ATP levels, leading to membrane depolarization. This depolarization triggers the opening of voltage-gated calcium channels, resulting in calcium influx into the cells.

Citation: Burger H (2023) The Pancreatic INS-1E Beta Cells’ Activation of the TRPV4 Channel Increases the Release of Insulin in Response to Glucose Through Calcium-Dependent Processes. J Clin Diabetes 7: 176.

Copyright: © 2023 Burger H. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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