Pancreatic islet metabolism and redox state during stimulation of insulin secretion with glucose and fructose

1984 ◽  
Vol 21 (4) ◽  
pp. 365-374 ◽  
Author(s):  
Kirsten Capito ◽  
Carl Jørgen Hedeskov ◽  
Jannik Landt ◽  
Peter Thams
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Redox State ◽  
Islet Metabolism ◽  
Stimulation Of

Stimulation of residual insulin secretion by glibenclamide in insulin dependent diabetics

1980 ◽  
Vol 95 (3) ◽  
pp. 372-375 ◽  
Author(s):  
B. J. Burke ◽  
R. J. Sherriff
Keyword(s):  
Insulin Secretion ◽  
Insulin Therapy ◽  
Metabolic Control ◽  
C Peptide ◽  
Beneficial Effects ◽  
Insulin Dependent ◽  
Serum And Urine ◽  
Stimulation Of

Abstract. Residual insulin secretion, reflected by the presence of C-peptide in serum and urine, has been demonstrated in 5 of 10 insulin-requiring diabetics of less than 10 years' duration tested. The C-peptide response, in the C-peptide secretors, showed a significant increase in both serum and urine after 4 weeks' treatment with 15 mg glibenclamide daily in addition to their usual insulin regime although no beneficial effects in metabolic control were detected. It is suggested that glibenclamide might be a useful adjunct to insulin therapy in insulinrequiring diabetics who still secrete C-peptide.

Synchronized Microfluidic System to Dynamically Assess Pancreatic Islet Function beyond Glucose-Stimulated Insulin Secretion

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2162-P
Author(s):  
STEPHAN NIEUWOUDT ◽  
RUTH MCDOWELL ◽  
HUI ZHANG ◽  
JOHN P. KIRWAN
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Microfluidic System ◽  
Islet Function ◽  
Glucose Stimulated Insulin Secretion

Stimulation of insulin secretion from isolated rat islets by SaRI 59-801

Diabetes ◽  
1985 ◽  
Vol 34 (6) ◽  
pp. 548-552 ◽  
Author(s):  
R. L. Hanson ◽  
C. M. Isaacson ◽  
L. D. Boyajy
Keyword(s):  
Insulin Secretion ◽  
Rat Islets ◽  
Isolated Rat Islets ◽  
Isolated Rat ◽  
Stimulation Of

scholarly journals GPR40 Is Necessary but Not Sufficient for Fatty Acid Stimulation of Insulin Secretion In Vivo

Diabetes ◽  
2007 ◽  
Vol 56 (4) ◽  
pp. 1087-1094 ◽  
Author(s):  
M. G. Latour ◽  
T. Alquier ◽  
E. Oseid ◽  
C. Tremblay ◽  
T. L. Jetton ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Fatty Acid ◽  
Insulin Secretion In Vivo ◽  
Stimulation Of

scholarly journals GRK2 contributes to glucose mediated calcium responses and insulin secretion in pancreatic islet cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jonathan Snyder ◽  
Atreju I Lackey ◽  
G. Schuyler Brown ◽  
Melisa Diaz ◽  
Tian Yuzhen ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Cell Model ◽  
Metabolic Phenotype ◽  
Atp Production ◽  
Pancreatic Islets Of Langerhans ◽  
Cardiac Mitochondrion ◽  
Pre Treatment ◽  
Insulin Responses

AbstractDiabetes is a metabolic syndrome rooted in impaired insulin and/or glucagon secretory responses within the pancreatic islets of Langerhans (islets). Insulin secretion is primarily regulated by two key factors: glucose-mediated ATP production and G-protein coupled receptors (GPCRs) signaling. GPCR kinase 2 (GRK2), a key regulator of GPCRs, is reported to be downregulated in the pancreas of spontaneously obesogenic and diabetogenic mice (ob/ob). Moreover, recent studies have shown that GRK2 non-canonically localizes to the cardiac mitochondrion, where it can contribute to glucose metabolism. Thus, islet GRK2 may impact insulin secretion through either mechanism. Utilizing Min6 cells, a pancreatic ß-cell model, we knocked down GRK2 and measured glucose-mediated intracellular calcium responses and insulin secretion. Silencing of GRK2 attenuated calcium responses, which were rescued by pertussis toxin pre-treatment, suggesting a Gαi/o-dependent mechanism. Pancreatic deletion of GRK2 in mice resulted in glucose intolerance with diminished insulin secretion. These differences were due to diminished insulin release rather than decreased insulin content or gross differences in islet architecture. Furthermore, a high fat diet feeding regimen exacerbated the metabolic phenotype in this model. These results suggest a new role for pancreatic islet GRK2 in glucose-mediated insulin responses that is relevant to type 2 diabetes disease progression.

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