Distinct roles for insulin and insulin-like growth factor-1 receptors in pancreatic β-cell glucose sensing revealed by RNA silencing

2004 ◽  
Vol 383 (3) ◽  
pp. 599-599
Author(s):  
G. da SILVA XAVIER ◽  
Q. QIAN ◽  
P. J. CULLEN ◽  
G. A. RUTTER
Keyword(s):  
Growth Factor ◽  
Rna Silencing ◽  
Glucose Sensing ◽  
Insulin Like Growth Factor ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Glucose

scholarly journals Role of Insulin-Like Growth Factor-Binding Protein 5 (IGFBP5) in Organismal and Pancreatic β-Cell Growth

2010 ◽  
Vol 24 (1) ◽  
pp. 178-192 ◽  
Author(s):  
Catherine E. Gleason ◽  
Yun Ning ◽  
Tara P. Cominski ◽  
Rana Gupta ◽  
Klaus H. Kaestner ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Binding Protein ◽  
Insulin Like Growth Factor ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Factor Binding

scholarly journals Distinct roles for insulin and insulin-like growth factor-1 receptors in pancreatic beta-cell glucose sensing revealed by RNA silencing

2004 ◽  
Vol 377 (1) ◽  
pp. 149-158 ◽  
Author(s):  
Gabriela da SILVA XAVIER ◽  
Qingwen QIAN ◽  
Peter J. CULLEN ◽  
Guy A. RUTTER
Keyword(s):  
Gene Expression ◽  
Insulin Secretion ◽  
Growth Factor ◽  
Rna Silencing ◽  
Pancreatic Beta Cell ◽  
Regulation Of Gene Expression ◽  
Glucose Sensing ◽  
Insulin Like Growth Factor ◽  
Β Cells ◽  
Elevated Glucose

The importance of the insulin receptor (IR) and the insulin-like growth factor-1 receptor (IGF-1R) for glucose-regulated insulin secretion and gene expression in pancreatic islet β-cells is at present unresolved. Here, we have used small interfering RNAs (siRNAs) to silence the expression of each receptor selectively in clonal MIN6 β-cells. Reduction of IR levels by >90% completely inhibited glucose (30 mM compared with 3 mM)-induced insulin secretion, but had no effect on depolarization-stimulated secretion. IR depletion also blocked the accumulation of preproinsulin (PPI), pancreatic duodenum homoeobox-1 (PDX-1) and glucokinase (GK) mRNAs at elevated glucose concentrations, as assessed by quantitative real-time PCR analysis (TaqMan®). Similarly, depletion of IGF-1R inhibited glucose-induced insulin secretion but, in contrast with the effects of IR silencing, had little impact on the regulation of gene expression by glucose. Moreover, loss of IGF-1R, but not IR, markedly inhibited glucose-stimulated increases in cytosolic and mitochondrial ATP, suggesting a role for IGF-1R in the maintenance of oxidative metabolism and in the generation of mitochondrial coupling factors. RNA silencing thus represents a useful tool for the efficient and selective inactivation of receptor tyrosine kinases in isolated β-cells. By inhibiting glucose-stimulated insulin secretion through the inactivation of IGF-1R, this approach also demonstrates the existence of insulin-independent mechanisms whereby elevated glucose concentrations regulate PPI, PDX-1 and GK gene expression in β-cells.

scholarly journals Insulin-like Growth Factor I (IGF-I)-stimulated Pancreatic β-Cell Growth Is Glucose-dependent

1998 ◽  
Vol 273 (28) ◽  
pp. 17771-17779 ◽  
Author(s):  
Sigrun R. Hügl ◽  
Morris F. White ◽  
Christopher J. Rhodes
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Insulin Like Growth Factor ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

Lactate overrides central nervous but not β-cell glucose sensing in humans

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

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.

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
Keyword(s):  
Glucose Sensing ◽  
Pancreatic Β Cell ◽  
Β Cell

scholarly journals Appropriate therapy for type 2 diabetes mellitus in view of pancreatic β-cell glucose toxicity: “the earlier, the better”

2015 ◽  
Vol 8 (2) ◽  
pp. 183-189 ◽  
Author(s):  
Hideaki Kaneto ◽  
Taka-aki Matsuoka ◽  
Tomohiko Kimura ◽  
Atsushi Obata ◽  
Masashi Shimoda ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Glucose Toxicity ◽  
Appropriate Therapy ◽  
Cell Glucose

scholarly journals Insulin-like Growth Factor 2 Overexpression Induces β-Cell Dysfunction and Increases Beta-cell Susceptibility to Damage

2015 ◽  
Vol 290 (27) ◽  
pp. 16772-16785 ◽  
Author(s):  
Alba Casellas ◽  
Cristina Mallol ◽  
Ariana Salavert ◽  
Veronica Jimenez ◽  
Miquel Garcia ◽  
...  
Keyword(s):  
Growth Factor ◽  
Beta Cell ◽  
Insulin Like Growth Factor ◽  
Β Cell ◽  
Cell Dysfunction
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