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 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.

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 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.

scholarly journals Beneficial Effect of Thymelaea hirsuta on Pancreatic Islet Degeneration, Renal Fibrosis, and Liver Damages as Demonstrated in Streptozotocin-Induced Diabetic Rat

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Sanae Abid ◽  
Hassane Mekhfi ◽  
Abderrahim Ziyyat ◽  
Abdekhaleq Legssyer ◽  
Mohammed Aziz ◽  
...  
Keyword(s):  
Pancreatic Islet ◽  
Renal Fibrosis ◽  
Islet Cell ◽  
Fasting Blood Glucose ◽  
Diabetic Rats ◽  
Medium Term ◽  
Pancreatic Islet Cell ◽  
Thymelaea Hirsuta ◽  
Hematoxylin And Eosin ◽  
Hematoxylin And Eosin Staining

Objective. In Morocco, Thymelaea hirsuta (T. hirsuta) (Thymelaeacea) is a medicinal plant widely used to treat and prevent diabetes. The present study aimed to evaluate the medium-term antidiabetic effect of aqueous extract (AqTh) and ethyl acetate fraction (EaTh) of Th and to investigate their putative protective effect on pancreatic islet degeneration, diabetic nephropathy, and liver damages in streptozotocin (STZ)-diabetic rats. Methods. Experimental diabetes in rats was induced by a single intraperitoneal injection of 50 mg/kg of STZ. During the treatment period (4 weeks), 200 mg/kg AqTh and 50 mg/kg EaTh were orally administrated daily to STZ-diabetic rats. A group of parameters including fasting blood glucose, biochemical parameters, and intestinal α-glucosidase inhibition were studied. Furthermore, histological study of the pancreas, kidney, liver, and aorta was also realized. Results. At the end of the treatment, both AqTh and EaTh had normalized fasting blood glucose to 1.08 and 1.25 g/l, respectively. AqTh has also reduced urinary creatinine and HbAc1. The EaTh showed inhibitory activity against intestinal α-glucosidase, whereas AqTh did not have this inhibitory effect. Furthermore, pancreas hematoxylin and eosin staining showed that AqTh or EaTh prevents pancreatic islet cell degeneration. As the same kidney, Masson’s trichrome staining has shown a significant prevention of renal fibrosis in AqTh- or EaTh-treated diabetic rats. On the other hand, liver hematoxylin and eosin staining showed that AqTh and EaTh prevent liver damage. Conclusion. We conclude that medium-term administration of AqTh and EaTh exerts significant antihyperglycemic effect in STZ-diabetic rats possibly through intestinal α-glucosidase inhibition and protection against pancreatic islet cell damage. Moreover, AqTh and EaTh treatment prevent nephropathy and liver complications in STZ-diabetic rats.

scholarly journals CXC chemokine ligand 12α-mediated increase in insulin secretion and survival of mouse pancreatic islets in response to oxidative stress through modulation of calcium uptake

2018 ◽  
Vol 70 (1) ◽  
pp. 191-204 ◽  
Author(s):  
Melita Vidakovic ◽  
Ernesto Caballero-Garrido ◽  
Mirjana Mihailovic ◽  
Jelena Arambasic-Jovanovic ◽  
Marija Sinadinovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Diabetes Diagnosis ◽  
Pancreatic Islet Cells ◽  
Pancreatic Cell ◽  
Cxcr4 Signaling

We examined whether CXCL12? improves insulin secretion by influencing the Ca2+ oscillation pattern and Ca2+ influx ([Ca2+]i), thereby enhancing the viability of pancreatic islet cells in oxidative stress. The islets of Langerhans were isolated from male OF1 mice and pretreated with 40 ng/mL of CXCL12? prior to exposure to 7.5 ?M hydrogen peroxide, which served to induce oxidative stress. Incubation of islets with CXCL12? induced pancreatic ?-cell proliferation and improved the ability of ?-cells to withstand oxidative stress. Consecutive treatments of isolated islets with hydrogen peroxide caused a decline in ?-cell functioning over time, while the CXCL12? pretreatment of islets exhibited a physiological response to high glucose that was comparable to control islets. The attenuated response of islets to a high D-glucose challenge was observed as a partial to complete abolishment of [Ca2+]i. Treatments with increasing concentrations of CXCL12? decreased the number of Ca2+ oscillations that lasted longer, thus pointing to an overall increase in [Ca2+]i, which was followed by increased insulin secretion. In addition, treatment of islets with CXCL12? enhanced the transcription rate for insulin and the CXCR4 gene, pointing to the importance of CXCL12/CXCR4 signaling in the regulation of Ca2+ intake and insulin secretion in pancreatic islet cells. We propose that a potential treatment with CXCL12? could help to remove preexisting glucotoxicity and associated temporary ?-cell stunning that might be present at the time of diabetes diagnosis in vivo.

Protection of Curcumin against Streptozocin-Induced Pancreatic Cell Destruction in T2D Rats

Planta Medica ◽  
2019 ◽  
Vol 86 (02) ◽  
pp. 113-120 ◽  
Author(s):  
Li Qihui ◽  
Deng Shuntian ◽  
Zhou Xin ◽  
Yu Xiaoxia ◽  
Chen Zhongpei
Keyword(s):  
Type 2 Diabetes ◽  
Blood Glucose ◽  
Signaling Pathway ◽  
Pancreatic Islet ◽  
Rat Model ◽  
Fasting Blood Glucose ◽  
Tissue Destruction ◽  
Β Cells ◽  
Pancreatic Cell

AbstractAs a kind of traditional Chinese medicine extract, curcumin has been proven to be effective in inhibiting inflammation and apoptosis in pancreatic islet β cells in the streptozotocin-induced diabetes mellitus rat model, although the underlying mechanism has not yet been clarified. To examine the effect of curcumin on inflammation and apoptosis in pancreatic islet β cells, we established a type 2 diabetes rat model by feeding the animals a high-fat diet and intraperitoneally injecting streptozotocin. The curcumin was administered by intraperitoneal injection. The rat body weight, fasting blood glucose, intraperitoneal glucose tolerance tests, and insulin tolerance tests were recorded and analyzed. Hematoxylin and eosin staining was used for morphological analysis, and a TUNEL assay was performed to detect the apoptotic cells. The expression levels of proteins related to oxidative stress, inflammation and apoptosis were detected by Western blotting and ELISA. Curcumin administration significantly decreased fasting blood glucose and promoted recovery of pancreas function in type 2 diabetes rats. In curcumin-treated rats, the pancreatic tissue destruction and apoptosis index were reduced. The expression of IL-1β, IL-6, TNF-α, caspase-3, Bax, and malondialdehyde were significantly reduced, and Bcl-2, superoxide dismutase 2, and glutathione peroxidase were significantly increased. Curcumin inhibited the expression of phosphorylated JNK and NF-κB proteins to block the RAGE/JNK/NF-κB signaling pathway. In conclusion, these results indicate that curcumin blocks the phosphorylation of JNK and NF-κB protein to inhibit this signaling pathway, thereby further inhibiting inflammation and apoptosis in pancreatic islet β cells. Curcumin has potential value for the treatment of diabetes.

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.

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.

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