scholarly journals Alloxan cytotoxicity in vitro. Microscope photometric analyses of Trypan Blue uptake by pancreatic islet cells in suspension

1977 ◽  
Vol 162 (1) ◽  
pp. 19-24 ◽  
Author(s):  
K Grankvist ◽  
Å Lernmark ◽  
I B Täljedal
Keyword(s):  
Pancreatic Islets ◽  
Beta Cells ◽  
Trypan Blue ◽  
Islet Cell ◽  
Visual Inspection ◽  
Islet Cells ◽  
Pancreatic Islet Cells ◽  
Cell Nuclei ◽  
20 Nm

Suspensions of islet cells were prepared by shaking pancreatic islets from non-inbred ob/ob mice in a Ca2+-free buffer. The cells were incubated with or without 20 mM-alloxan, and subsequently with Trypan Blue. The uptake of Trypan Blue by cell nuclei was analysed by microscope photometry and by counting the frequency of cells appearing stained on visual inspection. Cells classified as stained or unstained by inspection showed no overlap in nuclear absorbance. Suspensions not exposed to alloxan contained 70-80% of unstained cells. Alloxan markedly decreased the frequency of unstained cells, an effect counteracted by 5 or 20 mM-D-glucose. The spectrum of Trypan Blue in islet-cell nuclei was red-shifted by about 20 nm. A similar red-shift was observed on adding the dye to solutions of albumin or histones, but not on mixing the dye with DNA. Binding to basic proteins may explain the concentrative uptake of Trypan Blue in dead cells and contribute to the oncogenic transformation of phagocytotically active cells. Beta-Cells in vitro are killed by alloxan and hence represent a valid model for studying the diabetogenic action of the drug.

In vitro lymphocyte recognition of islet cells following in vivo priming with allogeneic murine pancreatic islets

1984 ◽  
Vol 105 (1) ◽  
pp. 87-92 ◽  
Author(s):  
Joanne Scott ◽  
Peter G. MacKay ◽  
Åke Lernmark
Keyword(s):  
Lymph Node ◽  
Pancreatic Islets ◽  
Islet Cell ◽  
Islet Cells ◽  
Culture Conditions ◽  
Pancreatic Tissue ◽  
Insulin Dependent ◽  
Lymph Node Cells

Abstract. Lymphocytes from patients with insulin-dependent diabetes have been shown to be sensitized to pancreatic tissue antigens. Mice immunized with homologous pancreatic islets have been found to develop glucose intolerance and insulitis. Since lymphocytes may be involved in diabetogenesis, we wished to determine if lymph node cells from islet-immunized mice can recognize and respond to islet cells in vitro. A.TL female mice were immunized with an emulsion of BALB/c islet homogenate and complete Freund's adjuvant (CFA); sham-treated A.TL mice were injected with adjuvant and water. Mice were sacrificed 7–8 days later and the draining lymph nodes were removed. The lymph node cells were co-cultured with freshly prepared irradiated BALB/c islet cell, which served as stimulator cells. The co-cultures were incubated for 24–26 h at 37°C, followed by a 16 h [3H]thymidine (TdR) pulse. A significant proliferation of lymph node cells from islet-primed mice was induced during the in vitro stimulation with irradiated islet cells when compared with lymph node cells from sham-treated mice (P < 0.001). The response may be islet-cell-specific, since irradiated lymph node cells from BALB/c mice failed to proliferative response under the same culture conditions (P > 0.80).

scholarly journals The microsomal glucose-6-phosphatase enzyme of pancreatic islets

1988 ◽  
Vol 255 (2) ◽  
pp. 471-476 ◽  
Author(s):  
I D Waddell ◽  
A Burchell
Keyword(s):  
Pancreatic Islets ◽  
Phosphatase Activity ◽  
Pancreatic Islet ◽  
Islet Cell ◽  
Islet Cells ◽  
Pancreatic Islet Cells ◽  
Kinetic Characteristics ◽  
Immunological Properties ◽  
Cell Glucose ◽  
Phosphatase Enzyme

Microsomal fractions isolated from pancreatic islet cells were shown to contain high specific glucose-6-phosphatase activity. The islet-cell glucose-6-phosphatase enzyme has the same Mr (36,500), similar immunological properties and kinetic characteristics to the hepatic microsomal glucose-6-phosphatase enzyme.

scholarly journals Recent progress in pancreatic islet cell therapy

2021 ◽  
Vol 41 (1) ◽  
Author(s):  
Erinn Zixuan Sim ◽  
Nobuaki Shiraki ◽  
Shoen Kume
Keyword(s):  
Stem Cells ◽  
Pancreatic Islet ◽  
Islet Cell ◽  
Recent Progress ◽  
Disease Modeling ◽  
Islet Cells ◽  
Pancreatic Islet Cells ◽  
Pancreatic Islet Cell

AbstractHuman pluripotent stem cells (PSCs), including human embryonic stem cells and induced pluripotent stem cells, are promising cell sources in regenerating pancreatic islets through in vitro directed differentiation. Recent progress in this research field has made it possible to generate glucose-responsive pancreatic islet cells from PSCs. Single-cell RNA sequencing techniques have been applied to analyze PSC-derived endocrine beta-cells, which are then compared with human islets. This has led to the identification of novel signaling pathways and molecules involved in lineage commitment during pancreatic differentiation and maturation processes. Single-cell transcriptomics are also used to construct a detailed map of in vivo endocrine differentiation of developing mouse embryos to study pancreatic islet development. Mimicking those occurring in vivo, it was reported that differentiating PSCs can generate similar islet cell structures, while metabolomics analysis highlighted key components involved in PSC-derived pancreatic islet cell function, providing information for the improvement of in vitro pancreatic maturation procedures. In addition, cell transplantation into diabetic animal models, together with the cell delivery system, is studied to ensure the therapeutic potentials of PSC-derived pancreatic islet cells. Combined with gene-editing technology, the engineered mutation-corrected PSC lines originated from diabetes patients could be differentiated into functional pancreatic islet cells, suggesting possible autologous cell therapy in the future. These PSC-derived pancreatic islet cells are a potential tool for studies of disease modeling and drug testing. Herein, we outlined the directed differentiation procedures of PSC-derived pancreatic islet cells, novel findings through transcriptome and metabolome studies, and recent progress in disease modeling.

Efficient gene transfer to dispersed human pancreatic islet cells in vitro using adenovirus-polylysine/DNA complexes or polycationic liposomes

Diabetes ◽  
1996 ◽  
Vol 45 (9) ◽  
pp. 1197-1203 ◽  
Author(s):  
J. Saldeen ◽  
D. T. Curiel ◽  
D. L. Eizirik ◽  
A. Andersson ◽  
E. Strandell ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Pancreatic Islet Cells ◽  
Dna Complexes ◽  
Human Pancreatic Islet ◽  
Efficient Gene

scholarly journals Immunohistochemistry of Pancreatic Islet Cell Tumors in the Ferret (Mustela putorius furo)

1997 ◽  
Vol 34 (5) ◽  
pp. 387-393 ◽  
Author(s):  
G. A. Andrews ◽  
N. C. Myers ◽  
C. Chard-Bergstrom
Keyword(s):  
Pancreatic Islets ◽  
Pancreatic Islet ◽  
Pancreatic Polypeptide ◽  
Islet Cell ◽  
Islet Cells ◽  
Neuron Specific Enolase ◽  
Islet Cell Tumors ◽  
Pancreatic Islet Cell ◽  
Formalin Fixed Paraffin Embedded ◽  
Pancreatic Islet Cell Tumors

Twenty-two pancreatic islet cell tumors and normal pancreatic islets from ferrets were evaluated by immunohistochemistry for expression of the peptide hormones insulin, somatostatin, glucagon, and pancreatic polypeptide (PP) and the neuroendocrine markers chromogranin A (CgA) and neuron-specific enolase (NSE). In normal pancreatic islets, the majority of cells stained strongly with CgA and NSE. A cells, B cells, D cells, and PP cells stained strongly with glucagon, insulin, somatostatin, and PP, respectively. All 22 tumors stained with CgA and NSE. The proportion of cells within tumors staining for CgA was variable, but more than half of the cells stained positively in 18 of the tumors. The intensity of staining for CgA was strong (reactivity equivalent to or greater than normal islet cells in adjacent tissue) in 11 moderate in six, and weak in five of the tumors. All tumors stained for NSE, with ≥50% of the cells staining in 21 of the tumors, and the intensity of staining was strong in 18 of the tumors. Twenty of 22 tumors stained positively for insulin, with ≥50% of the cells staining in 19 of them. The intensity of staining for insulin was strong in 12, moderate in seven, and weak in one of the tumors. Approximately ≤1% of the cells in 15 of 22 tumors stained for somatostatin, five tumors stained for pancreatic polypeptide, and three tumors stained for glucagon. These data indicate that the majority of islet cell tumors of ferrets express immunohistochemically detectable insulin. CgA and NSE are both useful general markers for such tumors, including those that are insulin negative. Commercially available antisera to CgA, NSE, insulin, glucagon, somatostatin, and PP work well in formalin-fixed, paraffin-embedded tissue for immunophenotyping islet cell tumors in the ferret.

Islet Cell Transplantation: In Vivo and in Vitro Functional Assessment of Nonhuman Primate Pancreatic Islets

2000 ◽  
Vol 9 (3) ◽  
pp. 409-414 ◽  
Author(s):  
Alessandra Rammcoli ◽  
Nicola Cautero ◽  
Camillo Ricordi ◽  
Michele Masetti ◽  
Ruth D. Molano ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Cell Transplantation ◽  
Functional Assessment ◽  
Nonhuman Primate ◽  
Islet Cell ◽  
Islet Cell Transplantation

Dietary fatty acids modify insulin secretion of rat pancreatic islet cells in vitro

2002 ◽  
Vol 25 (5) ◽  
pp. 436-441 ◽  
Author(s):  
F. J. Tinahones ◽  
A. Pareja ◽  
F. J. Soriguer ◽  
J. M. Gómez-Zumaquero ◽  
F. Cardona ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Dietary Fatty Acids ◽  
Pancreatic Islet Cells ◽  
Rat Pancreatic Islet

Role of the Interventional Radiologist in Pancreatic Whole Organ and Islet Cell Transplantation

2019 ◽  
Vol 03 (04) ◽  
pp. 314-325
Author(s):  
Ketan Y. Shah ◽  
Russell O. Simpson ◽  
Yifan Wang ◽  
Obi T. Okoye ◽  
Mithil B. Pandhi ◽  
...  
Keyword(s):  
Cell Transplantation ◽  
Islet Cell ◽  
Islet Cells ◽  
Portal System ◽  
Cell Transplant ◽  
Pancreatic Islet Cells ◽  
Islet Cell Transplantation ◽  
Image Guided ◽  
Treatment Of Diabetes

AbstractPancreas transplantation is an exciting therapy which has been used for several decades in the treatment of diabetes mellitus. It can be performed as either a whole organ or islet cell transplant. The role of interventional radiologists in the management of whole organ transplants is evolving and includes treatment of postoperative complications and graft biopsy to evaluate for rejection. An in-depth understanding of the transplant anatomy and variations is a fundamental tool in performing these interventions successfully. Islet cell transplantation entails delivery of purified donor pancreatic islet cells into the recipient portal vein. Because of their expertise in image-guided access to the portal system, interventional radiologists play a crucial role in this procedure. The purpose of this article is to review the indications, anatomy, complications, and outcomes of both whole organ and islet cell pancreas transplants, followed by a discussion of the role of interventional radiologists in each procedure.

Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro

2013 ◽  
Vol 228 (7) ◽  
pp. 1568-1576 ◽  
Author(s):  
Tamara Saksida ◽  
Ivana Nikolic ◽  
Milica Vujicic ◽  
Ulf J. Nilsson ◽  
Hakon Leffler ◽  
...  
Keyword(s):  
Pancreatic Islet ◽  
Islet Cells ◽  
Pancreatic Islet Cells ◽  
Galectin 3

Comparative toxicity of alloxan, N-alkylalloxans and ninhydrin to isolated pancreatic islets in vitro

1997 ◽  
Vol 155 (2) ◽  
pp. 283-293 ◽  
Author(s):  
A Jorns ◽  
R Munday ◽  
M Tiedge ◽  
S Lenzen
Keyword(s):  
Beta Cell ◽  
Pancreatic Islets ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Ultrastructural Changes ◽  
Cell Necrosis ◽  
High Concentrations ◽  
Beta Cell Necrosis

The in vitro toxicity of the diabetogenic agent alloxan as documented by the induction of beta cell necrosis was studied in isolated ob/ob mouse pancreatic islets. The effect of alloxan has been compared with that of a number of N-alkyl alloxan derivatives and with that of the structurally related compound, ninhydrin. Alloxan and its derivatives were selectively toxic to pancreatic beta cells, with other endocrine cells and exocrine parenchymal cells being well preserved, even at high concentration. In contrast, ninhydrin was selectively toxic to pancreatic beta cells only at comparatively low concentration, destroying all islet cell types at high concentrations. The ultrastructural changes induced by all the test compounds in pancreatic beta cells in vitro were very similar to those observed during the development of alloxan diabetes in vivo. The relative toxicity of the various compounds to pancreatic beta cells in vitro was not, however, related to their ability to cause diabetes in vivo. Indeed, the non-diabetogenic substances ninhydrin, N-butylalloxan and N-isobutylalloxan were very much more toxic to isolated islets than the diabetogenic compounds alloxan and N-methylalloxan. These results suggest that the differences in diabetogenicity among alloxan derivatives are not due to intrinsic differences in the susceptibility of the pancreatic beta cells to their toxicity, but may reflect differences in distribution or metabolism. High concentrations of glucose protected islets against the harmful effects of alloxan and its derivatives, but not those of ninhydrin. Low levels of glucose, and non-carbohydrate nutrients, afforded little protection, indicating that the effect of glucose is not due to the production of reducing equivalents within the cell, 3-O-Methylglucose, which protects against alloan diabetes in vivo, did not protect against alloxan toxicity in vitro. Since 3-O-methylglucose is known to prevent uptake of alloxan by pancreatic beta cells, it appears that uptake of alloxan by the cell is not a prerequisite for the induction of beta cell necrosis.

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