Silver Staining of Pancreatic Islets as Revealed by Electron Microscopy

1967 ◽  
Vol 25 ◽  
pp. 44-45
Author(s):  
Kazuaki Misugi ◽  
Nobuko Misugi ◽  
Hiroshi Yamada
Keyword(s):  
Pancreatic Islet ◽  
Silver Staining ◽  
Islet Cells ◽  
Severe Hypoglycemia ◽  
Granular Cell ◽  
Electron Microscopic Level ◽  
Staining Reaction ◽  
Electron Microscopic ◽  
Pancreatic Islet Cell ◽  
D Cell

The authors had described the fine structure of a type of pancreatic islet cell, which appeared different from typical alpha and beta cells, and tentatively considered that this third type of granular cell probably represents the D cell (Figure 1).Since silver staining has been widely used to differentiate different types of pancreatic islet cells by light microscopy, an attempt to examine this staining reaction at the electron microscopic level was made.Material and Method: Surgically removed specimens from three infants who suffered from severe hypoglycemia were used. The specimens were fixed and preserved in 20% neutral formalin. Frozen sections, 30 to 40 micron thick, were prepared and they were stained by Bielschowsky's method as modified by Suzuki (2). The stained sections were examined under a microscope and islet tissues were isolated. They were fixed in 1% osmium tetroxide in phosphate buffer for one hour and embedded in Epon 812 following dehydration through a series of alcohols and propylene oxide.

An experimental investigation into the possible origin of pancreatic islet cells from rhombencephalic neurectoderm

Development ◽  
1979 ◽  
Vol 52 (1) ◽  
pp. 23-38
Author(s):  
Ann Andrew ◽  
Beverley Kramer
Keyword(s):  
Pancreatic Islet ◽  
Islet Cell ◽  
Islet Cells ◽  
Cell Types ◽  
Nuclear Marker ◽  
Electron Microscopic ◽  
Pancreatic Islet Cell ◽  
Enteric Ganglia ◽  
Microscopic Features ◽  
Islet Cell Types

To determine whether or not any pancreatic islet cell type arises from rhombencephalic levels of neurectoderm, lengths of presumptive rhombencephalon (containing potential neural crest) of Black Australorp chick embryos at 6- to 9-somite stages were replaced isotopically and isochronically by neural tube of Japanese quail embryos. Some transplants included mesencephalic regions. In some cases various levels of the rhombencephalon were deleted and not replaced. The quail nuclear marker was detected in cranial ganglia in operated embryos sacrificed at 3¾ days of incubation and in enteric ganglia and cells accompanying some pancreatic nerves, in embryos killed at 7 days of incubation. This provided evidence of normal migration of crest cells from the grafts. Dopa was administered to the younger embryos, which were submitted to the formaldehyde-induced fluorescence procedure to demonstrate APUD (Amine Precursor Uptake and Decarboxylation) cells. No pancreatic APUD cells exhibited the quail nuclear marker. In 9- to 11-day embryos, A and B cells were identified by specific light and electron microscopic features. None showed the quail marker. The marker was also absent from those D cells seen and from cells of an as yet unidentified type, but not enough of these were found to warrant a conclusion. All islet cell types were found in embryos from which various levels of the rhombencephalon had been deleted. It is concluded that at least A and B islet cells are not derived from the rhombencephalic neurectoderm and probably not from mesencephalic levels. Their most likely origin remains the endoderm, which was the accepted source until recently

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.

Transcriptional activation of the rat glucagon gene by the cyclic AMP-responsive element in pancreatic islet cells

1990 ◽  
Vol 10 (12) ◽  
pp. 6799-6804
Author(s):  
W Knepel ◽  
J Chafitz ◽  
J F Habener
Keyword(s):  
Cyclic Amp ◽  
Pancreatic Islet ◽  
Transcriptional Activation ◽  
Islet Cells ◽  
Pancreatic Islet Cell ◽  
Heterologous Promoter ◽  
Dependent Protein Kinase ◽  
Dependent Protein ◽  
Flanking Region ◽  
Responsive Element

The 5'-flanking region of the rat glucagon gene contains, from nucleotides -291 to -298, a sequence (TGA CGTCA) which mediates cyclic AMP (cAMP) responsiveness in several genes (cAMP-responsive element [CRE]). However, because of nonpermissive bases surrounding the CRE octamer, the glucagon CRE does not confer cAMP responsiveness to an inert heterologous promoter in placental JEG cells that do not express the glucagon gene. This report describes transient transfection experiments with glucagon-reporter fusion genes that show that glucagon gene expression is activated by cAMP-dependent protein kinase A in a glucagon-expressing pancreatic islet cell line. This activation is mediated through the glucagon CRE.

scholarly journals Transcriptional activation of the rat glucagon gene by the cyclic AMP-responsive element in pancreatic islet cells.

1990 ◽  
Vol 10 (12) ◽  
pp. 6799-6804 ◽  
Author(s):  
W Knepel ◽  
J Chafitz ◽  
J F Habener
Keyword(s):  
Cyclic Amp ◽  
Pancreatic Islet ◽  
Transcriptional Activation ◽  
Islet Cells ◽  
Pancreatic Islet Cell ◽  
Heterologous Promoter ◽  
Dependent Protein Kinase ◽  
Dependent Protein ◽  
Flanking Region ◽  
Responsive Element

The 5'-flanking region of the rat glucagon gene contains, from nucleotides -291 to -298, a sequence (TGA CGTCA) which mediates cyclic AMP (cAMP) responsiveness in several genes (cAMP-responsive element [CRE]). However, because of nonpermissive bases surrounding the CRE octamer, the glucagon CRE does not confer cAMP responsiveness to an inert heterologous promoter in placental JEG cells that do not express the glucagon gene. This report describes transient transfection experiments with glucagon-reporter fusion genes that show that glucagon gene expression is activated by cAMP-dependent protein kinase A in a glucagon-expressing pancreatic islet cell line. This activation is mediated through the glucagon CRE.

scholarly journals Pancreatic islet cell autophagy during aging in rats

2013 ◽  
Vol 36 (2) ◽  
pp. 72 ◽  
Author(s):  
Shuang Wang ◽  
Qian-qian Sun ◽  
Bing Xiang ◽  
Xiu-Jun Li
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose ◽  
Pancreatic Islet ◽  
Islet Cell ◽  
Islet Cells ◽  
Cell Structure ◽  
Fasting Blood Glucose ◽  
Pancreatic Islet Cell ◽  
Pancreatic Cell ◽  
Old Rats

Purpose: Autophagy induces pancreatic β cell death. The purpose of the present study was to examine the hypothesis that the extent of pancreatic autophagy is associated with aging and age-related diabetes. Methods: Pancreatic tissue and blood samples were collected from Sprague Dawley rats receiving a normal diet at 2 (the young group), 6 (the adult group), 12 (the middle-age group) and 20-24 (the aged group) months of age. Body weight and fasting blood glucose, serum lipid levels and serum insulin levels were determined. Pancreatic cell structure and autophagy were determined using transmission electron microscopy of rats at 6, 12 and 24 months of age. Lamp2 and LC3b protein expression levels were determined by both immunohistochemistry and Western blot analyses, and islet cell apoptosis was assessed using the TUNEL assay. Results: Fasting blood glucose, triglyceride and FFA levels increased significantly with age (p < 0.05). Compared with levels seen in two-month-old rats, insulin secretion of islet cells in vitro was significantly reduced at 6, 12, and 20 months of age (p < 0.05). Autophagosomes were only observed in islet cells of 24 month-old rats. Increased expression of the autophagic markers, Lamp2 and LC3b, was observed with age. A significant increase in apoptotic index was observed between young rats (two-months-old) and older rats (six-, 12- and 24-months-old), but no differences were observed between rats six, 12 and 24 months of age. Conclusion: Appearance of autophagosomes and increased Lamp2 and LC3b expression in pancreatic islet cells coincided with a significant decrease in insulin secretion and elevation of fasting blood glucose in aged rats.

scholarly journals Potential Benefits of Nrf2/Keap1 Targeting in Pancreatic Islet Cell Transplantation

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 321 ◽  
Author(s):  
Alberto Jarrin Lopez ◽  
Hien Lau ◽  
Shiri Li ◽  
Hirohito Ichii
Keyword(s):  
Cell Transplantation ◽  
Pancreatic Islet ◽  
Islet Cell ◽  
Islet Cells ◽  
Therapeutic Option ◽  
Inflammatory Cells ◽  
Cell Integrity ◽  
Islet Cell Transplantation ◽  
Pancreatic Islet Cell ◽  
Antioxidant Genes

Permanent pancreatic islet cell destruction occurs in type 1 diabetes mellitus (T1DM) through the infiltration of inflammatory cells and cytokines. Loss of β-cell integrity secondary to oxidation leads to an inability to appropriately synthesize and secrete insulin. Allogenic islet cell transplantation (ICT) has risen as a therapeutic option to mitigate problematic hypoglycemia. Nevertheless, during the process of transplantation, islet cells are exposed to oxidatively caustic conditions that severely decrease the islet cell yield. Islet cells are at a baseline disadvantage to sustain themselves during times of metabolic stress as they lack a robust anti-oxidant defense system, glycogen stores, and vascularity. The Nrf2/Keap1 system is a master regulator of antioxidant genes that has garnered attention as pharmacologic activators have shown a protective response and a low side effect profile. Herein, we present the most recently studied Nrf2/Keap1 activators in pancreas for application in ICT: Dh404, dimethyl fumarate (DMF), and epigallocatechin gallate (EGCG). Furthermore, we discuss that Nrf2/Keap1 is a potential target to ameliorate oxidative stress at every step of the Edmonton Protocol.

Sign in / Sign up

Export Citation Format

Share Document