Further evidence that Zn2+ blocks voltage-dependent Ca2+ channels in the mouse pancreatic β-cell

1985 ◽  
Vol 13 (4) ◽  
pp. 680-681 ◽  
Author(s):  
ROSA FERRER ◽  
SALVADOR SALA ◽  
JUAN VICENTE SANCHEZ-ANDRES ◽  
BERNAT SORIA
Keyword(s):  
Pancreatic Β Cell ◽  
Β Cell ◽  
Voltage Dependent ◽  
Ca2 Channels

scholarly journals Cyanidin Stimulates Insulin Secretion and Pancreatic β-Cell Gene Expression through Activation of l-type Voltage-Dependent Ca2+ Channels

Nutrients ◽  
2017 ◽  
Vol 9 (8) ◽  
pp. 814 ◽  
Author(s):  
Tanyawan Suantawee ◽  
Sara Elazab ◽  
Walter Hsu ◽  
Shaomian Yao ◽  
Henrique Cheng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Secretion ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Voltage Dependent ◽  
Cell Gene Expression ◽  
Cell Gene ◽  
Ca2 Channels

scholarly journals Isoform-specific regulation of mood behavior and pancreatic β cell and cardiovascular function by L-type Ca2+ channels

2004 ◽  
Vol 113 (10) ◽  
pp. 1430-1439 ◽  
Author(s):  
Martina J. Sinnegger-Brauns ◽  
Alfred Hetzenauer ◽  
Irene G. Huber ◽  
Erik Renström ◽  
Georg Wietzorrek ◽  
...  
Keyword(s):  
Cardiovascular Function ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Specific Regulation ◽  
Ca2 Channels

scholarly journals Tetraspanin‐7 regulation of L‐type voltage‐dependent calcium channels controls pancreatic β‐cell insulin secretion

2020 ◽  
Vol 598 (21) ◽  
pp. 4887-4905 ◽  
Author(s):  
Matthew T. Dickerson ◽  
Prasanna K. Dadi ◽  
Regan B. Butterworth ◽  
Arya Y. Nakhe ◽  
Sarah M. Graff ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Calcium Channels ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Tetraspanin 7

Adipokines as key players in β cell function and failure

2019 ◽  
Vol 133 (22) ◽  
pp. 2317-2327 ◽  
Author(s):  
Nicolás Gómez-Banoy ◽  
James C. Lo
Keyword(s):  
Metabolic Diseases ◽  
Cell Function ◽  
Whole Body ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Axis ◽  
Β Cell Function ◽  
Prevalence Of Obesity ◽  
Specific Factors ◽  
Whole Body Metabolism

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.

INCRETIN AND DIABETES

2011 ◽  
pp. 5-10
Author(s):  
Huu Dang Tran
Keyword(s):  
Type 2 Diabetes ◽  
Cell Proliferation ◽  
Glycaemic Control ◽  
Animal Studies ◽  
Dipeptidyl Peptidase ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Glucose Sensitivity ◽  
Cell Glucose

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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