scholarly journals Mechanisms of glucose sensing in the pancreatic β-cell

Islets ◽  
2011 ◽  
Vol 3 (5) ◽  
pp. 224-230 ◽  
Author(s):  
Leonid E. Fridlyand ◽  
Louis H. Phillipson
2008 ◽  
Vol 49 (4) ◽  
pp. 814-822 ◽  
Author(s):  
Frederique Diraison ◽  
Magalie A. Ravier ◽  
Sarah K. Richards ◽  
Richard M. Smith ◽  
Hitoshi Shimano ◽  
...  

2008 ◽  
Vol 295 (6) ◽  
pp. E1298-E1306 ◽  
Author(s):  
Marcia Hiriart ◽  
Lydia Aguilar-Bryan

Mammalian β-cells are acutely and chronically regulated by sensing surrounding glucose levels that determine the rate at which insulin is secreted, to maintain euglycemia. Experimental research in vitro and in vivo has shown that, when these cells are exposed to adverse conditions like long periods of hypoglycemia or hyperglycemia, their capability to sense glucose is decreased. Understanding the normal physiology and identifying the main players along this route becomes paramount. In this review, we have taken on the task of looking at the role that ion channels play in the regulation of this process, delineating the different families, and describing the signaling that parallels the glucose sensing process that results in insulin release.


2015 ◽  
Vol 466 (2) ◽  
pp. 203-218 ◽  
Author(s):  
Guy A. Rutter ◽  
Timothy J. Pullen ◽  
David J. Hodson ◽  
Aida Martinez-Sanchez

By synthesizing and releasing the anabolic hormone insulin, pancreatic beta cells are essential for normal blood glucose homeostasis in mammals. Here, we review recent advances in our understanding of how these cells respond to nutrients with the release of the hormone, and how this process becomes defective in type 2 diabetes mellitus.


2019 ◽  
Vol 133 (22) ◽  
pp. 2317-2327 ◽  
Author(s):  
Nicolás Gómez-Banoy ◽  
James C. Lo

Abstract The growing prevalence of obesity and its related metabolic diseases, mainly Type 2 diabetes (T2D), has increased the interest in adipose tissue (AT) and its role as a principal metabolic orchestrator. Two decades of research have now shown that ATs act as an endocrine organ, secreting soluble factors termed adipocytokines or adipokines. These adipokines play crucial roles in whole-body metabolism with different mechanisms of action largely dependent on the tissue or cell type they are acting on. The pancreatic β cell, a key regulator of glucose metabolism due to its ability to produce and secrete insulin, has been identified as a target for several adipokines. This review will focus on how adipokines affect pancreatic β cell function and their impact on pancreatic β cell survival in disease contexts such as diabetes. Initially, the “classic” adipokines will be discussed, followed by novel secreted adipocyte-specific factors that show therapeutic promise in regulating the adipose–pancreatic β cell axis.


2008 ◽  
Vol 116 (09) ◽  
Author(s):  
SM Schmid ◽  
M Hallschmid ◽  
K Jauch-Chara ◽  
KM Oltmanns ◽  
A Peters ◽  
...  
Keyword(s):  
Β Cell ◽  

2011 ◽  
pp. 5-10
Author(s):  
Huu Dang Tran

The incretins are peptide hormones secreted from the gut in response to food. They increase the secretion of insulin. The incretin response is reduced in patients with type 2 diabetes so drugs acting on incretins may improve glycaemic control. Incretins are metabolised by dipeptidyl peptidase, so selectively inhibiting this enzyme increases the concentration of circulating incretins. A similar effect results from giving an incretin analogue that cannot be cleaved by dipeptidyl peptidase. Studies have identified other actions including improvement in pancreatic β cell glucose sensitivity and, in animal studies, promotion of pancreatic β cell proliferation and reduction in β cell apoptosis.


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