scholarly journals The role of pyruvate carboxylase in insulin secretion and proliferation in rat pancreatic beta cells

Diabetologia ◽  
2008 ◽  
Vol 51 (11) ◽  
pp. 2022-2030 ◽  
Author(s):  
J. Xu ◽  
J. Han ◽  
Y. S. Long ◽  
P. N. Epstein ◽  
Y. Q. Liu
Keyword(s):  
Insulin Secretion ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Pyruvate Carboxylase

scholarly journals The Role of Phosphofructokinase-M (Pfkm) in Oscillatory Glycolysis and Insulin Secretion in Pancreatic Beta Cells

2019 ◽  
Vol 116 (3) ◽  
pp. 235a
Author(s):  
Vishal S. Parekh ◽  
Jim Ren ◽  
Leslie S. Satin
Keyword(s):  
Insulin Secretion ◽  
Beta Cells ◽  
Pancreatic Beta Cells

scholarly journals In vivo phosphoproteomics reveals pathogenic signaling changes in diabetic islets

2018 ◽  
Author(s):  
Francesca Sacco ◽  
Anett Seelig ◽  
Sean J. Humphrey ◽  
Natalie Krahmer ◽  
Francesco Volta ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Drug Targets ◽  
High Sensitivity ◽  
Glucose Stimulated Insulin Secretion

SUMMARYProgressive decline of pancreatic beta cells function is key to the pathogenesis of type 2 diabetes. Protein phosphorylation is the central mechanism controlling glucose-stimulated insulin secretion in beta cells. However, if and how signaling networks are remodeled in diabetic isletsin vivoremain unknowns. Here we applied high-sensitivity mass spectrometry-based proteomics and quantified the levels of about 6,500 proteins and 13,000 phosphopeptides in islets of obese diabetic mice and matched controls. This highlighted drastic remodeling of key kinase hubs and signaling pathways. We integrated our phosphoproteomic dataset with a literature-derived signaling network, which revealed a crucial and conserved role of GSK3 kinase in the control of the beta cells-specific transcription factor PDX1 and insulin secretion, which we functionally verified. Our resource will enable the community to investigate potential mechanisms and drug targets in type 2 diabetes.

Involvement of ATP-sensitive K+ channels in free radical-mediated inhibition of insulin secretion in rat pancreatic beta-cells

Diabetes ◽  
1995 ◽  
Vol 44 (8) ◽  
pp. 878-883 ◽  
Author(s):  
M. Nakazaki ◽  
M. Kakei ◽  
N. Koriyama ◽  
H. Tanaka
Keyword(s):  
Insulin Secretion ◽  
Free Radical ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
K Channels

scholarly journals Pancreatic beta-cells expressing the Arg64 variant of the beta(3)-adrenergic receptor exhibit abnormal insulin secretory activity

2001 ◽  
Vol 27 (2) ◽  
pp. 133-144 ◽  
Author(s):  
R Perfetti ◽  
H Hui ◽  
K Chamie ◽  
S Binder ◽  
M Seibert ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Beta Cells ◽  
Western Blotting ◽  
Adrenergic Receptor ◽  
Pancreatic Beta Cells ◽  
Secretory Activity ◽  
Host Cells ◽  
Human Pancreas ◽  
Dependent Manner ◽  
Wild Type

The Arg64 beta(3)-adrenergic receptor (beta(3)AR) variant is associated with an earlier age of onset of diabetes and lower levels of insulin secretion in humans. The aims of this study were to investigate whether beta(3)AR is expressed by islet cells, if receptor binding affects insulin secretion and, finally, if the beta(3)AR Arg64 variant induces abnormal insulin secretory activity. Human pancreas extracts were subjected to RT-PCR, Western blotting and immunostaining analyses. DNA sequencing and Western blotting demonstrated that the beta(3)AR gene is transcribed and translated in the human pancreas; immunostaining showed that it is expressed by the islets of Langerhans. Cultured rat beta-cells responded to human beta(3)AR agonists in a dose- and time-dependent manner. Transfection of cultured rat beta-cells with the wild-type human beta(3)AR produced an increased baseline and ligand-dependent insulin secretion compared with parental cells. On the other hand, cells transfected with the Arg64 variant of the beta(3)AR secreted less insulin, both spontaneously and after exposure to human beta(3)AR agonists. Furthermore, while transfection with the wild-type beta(3)AR preserved the glucose-dependent secretion of insulin, expression of the variant receptor rendered the host cells significantly less responsive to glucose. In summary, cells express the beta(3)AR, and its activation contributes to the regulation of insulin secretion. These findings may help explain the low levels of insulin secretion in response to an i.v. glucose tolerance test observed in humans carrying the Arg64 polymorphism.

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