INS-1 cell glucose-stimulated insulin secretion is reduced by the downregulation of the 67 kDa laminin receptor

2013 ◽  
Vol 9 (12) ◽  
pp. 1376-1385 ◽  
Author(s):  
Georges Sabra ◽  
Evan A. Dubiel ◽  
Carina Kuehn ◽  
Taoufik Khalfaoui ◽  
Jean-François Beaulieu ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Laminin Receptor ◽  
Glucose Stimulated Insulin Secretion ◽  
Cell Glucose

scholarly journals The Transcriptional Co-Regulator HCF-1 Is Required for INS-1 β-cell Glucose-Stimulated Insulin Secretion

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e78841 ◽  
Author(s):  
Terri N. Iwata ◽  
Timothy J. Cowley ◽  
Michael Sloma ◽  
Yewei Ji ◽  
Hana Kim ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Β Cell ◽  
Glucose Stimulated Insulin Secretion ◽  
Cell Glucose

scholarly journals Loss of AMP-activated protein kinase α2 subunit in mouse β-cells impairs glucose-stimulated insulin secretion and inhibits their sensitivity to hypoglycaemia

2010 ◽  
Vol 429 (2) ◽  
pp. 323-333 ◽  
Author(s):  
Craig Beall ◽  
Kaisa Piipari ◽  
Hind Al-Qassab ◽  
Mark A. Smith ◽  
Nadeene Parker ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Sensing ◽  
Whole Body ◽  
Β Cells ◽  
Β Cell ◽  
Glucose Homoeostasis ◽  
Low Glucose ◽  
Glucose Stimulated Insulin Secretion ◽  
Amp Activated Protein Kinase ◽  
Cell Glucose

AMPK (AMP-activated protein kinase) signalling plays a key role in whole-body energy homoeostasis, although its precise role in pancreatic β-cell function remains unclear. In the present stusy, we therefore investigated whether AMPK plays a critical function in β-cell glucose sensing and is required for the maintenance of normal glucose homoeostasis. Mice lacking AMPKα2 in β-cells and a population of hypothalamic neurons (RIPCreα2KO mice) and RIPCreα2KO mice lacking AMPKα1 (α1KORIPCreα2KO) globally were assessed for whole-body glucose homoeostasis and insulin secretion. Isolated pancreatic islets from these mice were assessed for glucose-stimulated insulin secretion and gene expression changes. Cultured β-cells were examined electrophysiologically for their electrical responsiveness to hypoglycaemia. RIPCreα2KO mice exhibited glucose intolerance and impaired GSIS (glucose-stimulated insulin secretion) and this was exacerbated in α1KORIPCreα2KO mice. Reduced glucose concentrations failed to completely suppress insulin secretion in islets from RIPCreα2KO and α1KORIPCreα2KO mice, and conversely GSIS was impaired. β-Cells lacking AMPKα2 or expressing a kinase-dead AMPKα2 failed to hyperpolarize in response to low glucose, although KATP (ATP-sensitive potassium) channel function was intact. We could detect no alteration of GLUT2 (glucose transporter 2), glucose uptake or glucokinase that could explain this glucose insensitivity. UCP2 (uncoupling protein 2) expression was reduced in RIPCreα2KO islets and the UCP2 inhibitor genipin suppressed low-glucose-mediated wild-type mouse β-cell hyperpolarization, mimicking the effect of AMPKα2 loss. These results show that AMPKα2 activity is necessary to maintain normal pancreatic β-cell glucose sensing, possibly by maintaining high β-cell levels of UCP2.

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

scholarly journals In Vitro Studies to Assess the α-Glucosidase Inhibitory Activity and Insulin Secretion Effect of Isorhamnetin 3-O-Glucoside and Quercetin 3-O-Glucoside Isolated from Salicornia herbacea

Processes ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 483
Author(s):  
Dahae Lee ◽  
Jun Yeon Park ◽  
Sanghyun Lee ◽  
Ki Sung Kang
Keyword(s):  
Insulin Secretion ◽  
Cell Function ◽  
Ethanolic Extract ◽  
Ethyl Acetate Fraction ◽  
Gradient Elution ◽  
Glucosidase Activity ◽  
Β Cell Function ◽  
Glucose Stimulated Insulin Secretion ◽  
Salicornia Herbacea

In this study, we examined the effect of ethanolic extract of Salicornia herbacea (ESH), isorhamnetin 3-O-glucoside (I3G), quercetin 3-O-glucoside (Q3G), quercetin, and isorhamnetin on α-glucosidase activity and glucose-stimulated insulin secretion (GSIS) in insulin-secreting rat insulinoma (INS-1) cells. A portion of the ethyl acetate fraction of ESH was chromatographed on a silica gel by a gradient elution with chloroform and methanol to provide Q3G and I3G. ESH, Q3G, and quercetin inhibited α-glucosidase activity, and quercetin (IC50 value was 29.47 ± 3.36 μM) inhibited the activity more effectively than Q3G. We further demonstrated that ESH, Q3G, quercetin, I3G, and isorhamnetin promote GSIS in INS-1 pancreatic β-cells without inducing cytotoxicity. Among them, I3G was the most effective in enhancing GSIS. I3G enhanced the phosphorylation of total extracellular signal-regulated kinase (ERK), insulin receptor substrate-2 (IRS-2), phosphatidylinositol 3-kinase (PI3K), Akt, and activated pancreatic and duodenal homeobox-1 (PDX-1), which are associated with insulin secretion and β-cell function. As components of ESH, Q3G has the potential to regulate blood glucose by inhibiting α-glucosidase activity, and I3G enhances the insulin secretion, but its bioavailability should be considered in determining biological importance.

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