scholarly journals The coupling of metabolic to secretory events in pancreatic islets. The cytosolic redox state

1984 ◽  
Vol 220 (2) ◽  
pp. 433-440 ◽  
Author(s):  
A Sener ◽  
F Malaisse-Lagae ◽  
S P Dufrane ◽  
W J Malaisse
Keyword(s):  
Pancreatic Islets ◽  
Malate Dehydrogenase ◽  
Insulin Release ◽  
Pancreatic Islet ◽  
Flow Rate ◽  
Isocitrate Dehydrogenase ◽  
Malic Enzyme ◽  
Redox State ◽  
Islet Cells ◽  
Pancreatic Islet Cells

NADP-linked isocitrate dehydrogenase and malic enzyme [malate dehydrogenase (decarboxylating) (NADP)] activities were characterized in the cytosol of pancreatic islet cells. D-Glucose and L-leucine augmented the cytosolic NADPH/NADP+ ratio, as judged from the isocitrate/2-oxoglutarate and malate/pyruvate islet contents. The flow rate through the malic enzyme was judged from the output of labelled pyruvate by islets exposed to either L-[U-14C]glutamine or L-[U-14C]leucine. The cytosolic generation of NADPH, e.g. at the level of the malic enzyme, may play a role in the coupling of metabolic to secretory events in the process of nutrient-stimulated insulin release.

scholarly journals Effect of glucose on the intracellular pH of pancreatic islet cells

1984 ◽  
Vol 218 (3) ◽  
pp. 887-892 ◽  
Author(s):  
P Lindström ◽  
J Sehlin
Keyword(s):  
Insulin Release ◽  
Intracellular Ph ◽  
Pancreatic Islet ◽  
Basal Insulin ◽  
Islet Cells ◽  
Maximum Effect ◽  
Maximal Effect ◽  
Pancreatic Islet Cells ◽  
Bicarbonate Buffer ◽  
Effect Of Glucose

To characterize the effect of glucose on the intracellular pH (pHi) of pancreatic islet cells, we measured the accumulation of 14C-labelled 5,5-dimethyloxazolidine-2,4-dione ([14C]DMO) in beta-cell-rich islets from ob/ob mice. D-Glucose (20 mM) stimulated insulin release and enhanced the [14C]DMO equilibrium uptake corresponding to an increase of pHi by about 0.15 unit. The glucose effect on DMO uptake was concentration-dependent, with half-maximal effect at about 4 mM-glucose and maximum effect at about 10 mM-glucose. It was inhibited by 20 mM-mannoheptulose and potentiated by 4 mM-L-5-hydroxytryptophan, but not affected by 2 mM-theophylline. Mannoheptulose is an inhibitor and L-5-hydroxytryptophan and theophylline are potentiators of glucose-stimulated insulin release. The glucose-induced increase in pHi appeared rapidly (7 min) and persisted for at least 30 min and it was observed both in bicarbonate/CO2-buffered and in Hepes [4-(2-hydroxyethyl)-1-piperazine-ethanesulphonic acid]-buffered media. Addition of extracellular bicarbonate buffer lowered the pHi, but did not affect basal insulin release, whereas 5 mM-NH4+ increased pHi and induced a 4-fold increase of basal insulin release. We conclude that, in contrast with previous assumptions, glucose increases intracellular pH in the islet cells. This effect may be coupled to the glucose metabolism and associated with triggering of insulin release.

The Possible Importance of Contact between Pancreatic Islet Cells for the Control of Insulin Release*

Endocrinology ◽  
1982 ◽  
Vol 111 (1) ◽  
pp. 86-94 ◽  
Author(s):  
PHILIPPE A. HALBAN ◽  
CLAES B. WOLLHEIM ◽  
BENIGNA BLONDEL ◽  
PAOLO MEDA ◽  
ERIC N. NIESOR ◽  
...  
Keyword(s):  
Insulin Release ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Pancreatic Islet Cells

scholarly journals Expression of Insulinoma-Associated 2 (INSM2) in Pancreatic Islet Cells Is Regulated by the Transcription Factors Ngn3 and NeuroD1

Endocrinology ◽  
2011 ◽  
Vol 152 (5) ◽  
pp. 1961-1969 ◽  
Author(s):  
Tao Cai ◽  
Xiang Chen ◽  
Rennian Wang ◽  
Huan Xu ◽  
Yuhui You ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Pancreatic Islets ◽  
Pancreatic Islet ◽  
Chromatin Immunoprecipitation ◽  
Islet Cells ◽  
Mouse Embryos ◽  
Pancreatic Islet Cells ◽  
Neurogenin 3 ◽  
Fetal Pancreas ◽  
E Boxes

The insulinoma-associated 2 (Insm2) gene is a member of the Snail/Gfi1/Insm1 transcriptional repressor superfamily. However, little is known about how the expression of human INSM2 or mouse Insm2 in neuroendocrine tissues is regulated. Here we report the expression of INSM2/Insm2 in human fetal pancreas and mouse embryos, as well as adult pancreatic islets, and its regulation by two major islet transcription factors. Mutagenesis and chromatin immunoprecipitation analysis demonstrated that the proximal E-boxes of the mouse Insm2 promoter are direct targets of neurogenin 3 and neurogenic differentiation 1 (NeuroD1). Furthermore, we found that endogenous Insm2 expression was activated in Ngn3/NeuroD1-transduced pancreatic epithelial duct cells. Our results suggest that Insm2 plays an important role in the differentiation cascade of Ngn3/NeuroD1 signaling in pancreatic islets.

scholarly journals Gatifloxacin Induces Augmented Insulin Release and Intracellular Insulin Depletion of Pancreatic Islet Cells

2007 ◽  
Vol 30 (4) ◽  
pp. 644-647 ◽  
Author(s):  
Takashi Tomita ◽  
Mariko Onishi ◽  
Eiji Sato ◽  
Yasuhiro Kimura ◽  
Kenji Kihira
Keyword(s):  
Insulin Release ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Pancreatic Islet Cells

Assembly of bioactive multilayered nanocoatings on pancreatic islet cells: incorporation of α1-antitrypsin into the coatings

2015 ◽  
Vol 51 (53) ◽  
pp. 10652-10655 ◽  
Author(s):  
Zheng-Liang Zhi ◽  
Jashandeep Singh ◽  
Amazon L. F. Austin ◽  
David C. D. Hope ◽  
Aileen J. King ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Pancreatic Islet ◽  
Inflammatory Reaction ◽  
Islet Cells ◽  
Therapeutic Proteins ◽  
Pancreatic Islet Cells ◽  
Glycol Chitosan ◽  
Multilayer Deposition

A novel multilayer deposition approach to the delivery of therapeutic proteins onto the surface of pancreatic islets, using a heparin polyaldehyde and glycol chitosan alternating layering scheme, has been developed for addressing the blood-mediated inflammatory reaction against islet cells.

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