scholarly journals In vitro insulin secretion by pancreatic tissue from infants with diazoxide-resistant congenital hyperinsulinism deviates from model predictions

2011 ◽  
Vol 121 (10) ◽  
pp. 3932-3942 ◽  
Author(s):  
Jean-Claude Henquin ◽  
Myriam Nenquin ◽  
Christine Sempoux ◽  
Yves Guiot ◽  
Christine Bellanné-Chantelot ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Tissue ◽  
Congenital Hyperinsulinism ◽  
Model Predictions ◽  
In Vitro Insulin Secretion

Hyperglycemic athymic nude mice: factors affecting in vitro insulin secretion

1992 ◽  
Vol 263 (6) ◽  
pp. E1131-E1133
Author(s):  
A. Zeidler ◽  
P. Edwards ◽  
J. Goldman ◽  
S. Kort ◽  
W. P. Meehan ◽  
...  
Keyword(s):  
Animal Model ◽  
Insulin Secretion ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Factors Affecting ◽  
In Vitro Insulin Secretion ◽  
Insulin Secretion In Vitro ◽  
And Control

The strain of athymic nude male mice (ANM) developed at the University of Southern California (USC) exhibits spontaneous hyperglycemia and relative hypoinsulinemia in vivo. To investigate factors that influence insulin secretion in this animal model of non-insulin-dependent diabetes mellitus, we utilized the isolated perfused mouse pancreas of the ANM-USC and control BALB/c mice. We compared in vitro glucose-induced insulin secretion in ANM-USC and control mice, inhibition of secretion by somatostatin, and variability of insulin secretion over the two-year period it took to complete these experiments. Glucose-induced insulin secretion from the isolated pancreas was biphasic in both ANM-USC and controls. Insulin secretion was quantitatively equal to or greater than control mice, depending on the phase of secretion analyzed and the source of the control mice. In contrast to pancreases of control mice, insulin secretion from ANM-USC pancreases was relatively resistant to inhibition of insulin secretion by somatostatin. Variability in insulin secretion over the two years in which these experiments were performed was greater from pancreases of control than that observed from pancreases of the ANM-USC. The hyperglycemic ANM-USC mouse does not demonstrate diminished insulin secretion in vitro yet is relatively hypoinsulinemic in vivo. Thus circulating factors other than somatostatin might contribute to the insulinopenic stage in this animal model.

scholarly journals Downregulation of lncRNA TUG1 Affects Apoptosis and Insulin Secretion in Mouse Pancreatic β Cells

2015 ◽  
Vol 35 (5) ◽  
pp. 1892-1904 ◽  
Author(s):  
Dan-dan Yin ◽  
Er-bao Zhang ◽  
Liang-hui You ◽  
Ning Wang ◽  
Lin-tao Wang ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Cell Function ◽  
Annexin V ◽  
Pancreatic Tissue ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells ◽  
Lncrna Tug1

Background: Increasing evidence indicates that long noncoding RNAs (IncRNAs) perform specific biological functions in diverse processes. Recent studies have reported that IncRNAs may be involved in β cell function. The aim of this study was to characterize the role of IncRNA TUG1 in mouse pancreatic β cell functioning both in vitro and in vivo. Methods: qRT-PCR analyses were performed to detect the expression of lncRNA TUG1 in different tissues. RNAi, MTT, TUNEL and Annexin V-FITC assays and western blot, GSIS, ELISA and immunochemistry analyses were performed to detect the effect of lncRNA TUG1 on cell apoptosis and insulin secretion in vitro and in vivo. Results: lncRNA TUG1 was highly expressed in pancreatic tissue compared with other organ tissues, and expression was dynamically regulated by glucose in Nit-1 cells. Knockdown of lncRNA TUG1 expression resulted in an increased apoptosis ratio and decreased insulin secretion in β cells both in vitro and in vivo . Immunochemistry analyses suggested decreased relative islet area after treatment with lncRNA TUG1 siRNA. Conclusion: Downregulation of lncRNA TUG1 expression affected apoptosis and insulin secretion in pancreatic β cells in vitro and in vivo. lncRNA TUG1 may represent a factor that regulates the function of pancreatic β cells.

Glucose responsiveness and acetylcholine sensitivity of pancreatic beta-cells after vagotomy

1984 ◽  
Vol 246 (6) ◽  
pp. R985-R993 ◽  
Author(s):  
L. A. Campfield ◽  
F. J. Smith ◽  
R. E. Eskinazi
Keyword(s):  
Insulin Secretion ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Acetylcholine Receptors ◽  
Sham Operation ◽  
Neural Input ◽  
Acetylcholine Sensitivity ◽  
Long Evans ◽  
In Vitro Insulin Secretion

The chronic effects of removal of parasympathetic neural input to the pancreas on in vitro insulin secretion were assessed. Groups of Wistar and Long-Evans rats received total subdiaphragmatic vagotomy or sham operation. Four to ten weeks later, after the return of food intake and body weight in the vagotomized groups to values similar to the sham-operated groups, pancreatic islets were isolated and statically incubated with selected concentrations of glucose and acetylcholine. Two experimental protocols were used. In the first experiment, insulin secretion in response to basal (5 mM) glucose was 59 +/- 15 (SE) and 65 +/- 13% greater in islets from the vagotomized Wistar and Long-Evans groups, respectively, than in the corresponding sham groups. The enhancement of insulin secretion by several doses of acetylcholine observed in islets from sham-operated groups was totally absent in islets from both vagotomized strains. In the second experiment, insulin secretion was determined in response to selected glucose concentrations by using islets from Wistar rats. An upward and leftward shift of the dose-response curve was observed in the vagotomized group causing 5 mM to become a stimulatory glucose concentration and increasing the stimulatory potency of 10 mM glucose. These results suggest that interruption of vagal input to pancreatic beta-cells may induce a compensatory increase in responsiveness to glucose and a functional suppression of acetylcholine receptors. These data provide further support for the hypothesis that vagal input plays a functionally important role in the control of insulin secretion and maintenance of acetylcholine sensitivity.

Insulin Secretion in vitro by Pancreatic Tissue from Normal, Adrenalectomized, and Cortisol-Treated Rats.

1967 ◽  
Vol 124 (3) ◽  
pp. 924-928 ◽  
Author(s):  
W. J. Malaisse ◽  
F. Malaisse-Lagae ◽  
E. F. Mc Craw ◽  
P. H. Wright
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Tissue ◽  
Insulin Secretion In Vitro
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