scholarly journals Pancreatic Ppy-expressing γ-cells display mixed phenotypic traits and the adaptive plasticity to engage insulin production

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Marta Perez-Frances ◽  
Léon van Gurp ◽  
Maria Valentina Abate ◽  
Valentina Cigliola ◽  
Kenichiro Furuyama ◽  
...  
Keyword(s):  
Islet Cell ◽  
Cell Injury ◽  
Therapeutic Potential ◽  
Cell Types ◽  
Adaptive Plasticity ◽  
Phenotypic Traits ◽  
Insulin Production ◽  
Pancreatic Islet Cell ◽  
Glucose Levels ◽  
Islet Cell Types

AbstractThe cellular identity of pancreatic polypeptide (Ppy)-expressing γ-cells, one of the rarest pancreatic islet cell-type, remains elusive. Within islets, glucagon and somatostatin, released respectively from α- and δ-cells, modulate the secretion of insulin by β-cells. Dysregulation of insulin production raises blood glucose levels, leading to diabetes onset. Here, we present the genetic signature of human and mouse γ-cells. Using different approaches, we identified a set of genes and pathways defining their functional identity. We found that the γ-cell population is heterogeneous, with subsets of cells producing another hormone in addition to Ppy. These bihormonal cells share identity markers typical of the other islet cell-types. In mice, Ppy gene inactivation or conditional γ-cell ablation did not alter glycemia nor body weight. Interestingly, upon β-cell injury induction, γ-cells exhibited gene expression changes and some of them engaged insulin production, like α- and δ-cells. In conclusion, we provide a comprehensive characterization of γ-cells and highlight their plasticity and therapeutic potential.

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 Single‐cell transcriptomes reveal characteristic features of human pancreatic islet cell types

EMBO Reports ◽  
2015 ◽  
Vol 17 (2) ◽  
pp. 178-187 ◽  
Author(s):  
Jin Li ◽  
Johanna Klughammer ◽  
Matthias Farlik ◽  
Thomas Penz ◽  
Andreas Spittler ◽  
...  
Keyword(s):  
Single Cell ◽  
Pancreatic Islet ◽  
Islet Cell ◽  
Cell Types ◽  
Pancreatic Islet Cell ◽  
Human Pancreatic Islet ◽  
Characteristic Features ◽  
Islet Cell Types

Distribution and density of melatonin receptors in human main pancreatic islet cell types

2018 ◽  
Vol 65 (1) ◽  
pp. e12480 ◽  
Author(s):  
Juliane Zibolka ◽  
Ivonne Bazwinsky-Wutschke ◽  
Eckhard Mühlbauer ◽  
Elmar Peschke
Keyword(s):  
Pancreatic Islet ◽  
Islet Cell ◽  
Cell Types ◽  
Melatonin Receptors ◽  
Pancreatic Islet Cell ◽  
Islet Cell Types

Simultaneous Assessment of Prohormone Transport and Processing in Four Separate Islet Cell Types

Pancreas ◽  
1988 ◽  
Vol 3 (6) ◽  
pp. 700-713 ◽  
Author(s):  
Bryan D. Noe ◽  
Mylene Amherdt ◽  
Alain Perrelet ◽  
Lelio Orci
Keyword(s):  
Islet Cell ◽  
Cell Types ◽  
Islet Cell Types ◽  
Simultaneous Assessment

scholarly journals Functional identification of islet cell types by electrophysiological fingerprinting

2017 ◽  
Vol 14 (128) ◽  
pp. 20160999 ◽  
Author(s):  
Linford J. B. Briant ◽  
Quan Zhang ◽  
Elisa Vergari ◽  
Joely A. Kellard ◽  
Blanca Rodriguez ◽  
...  
Keyword(s):  
Electrical Activity ◽  
Islet Cell ◽  
Cell Types ◽  
Cell Type ◽  
Functional Identification ◽  
Large Dataset ◽  
Intact Mouse ◽  
Whole Cell Patch Clamp ◽  
Mouse Islets ◽  
Islet Cell Types

The α-, β- and δ-cells of the pancreatic islet exhibit different electrophysiological features. We used a large dataset of whole-cell patch-clamp recordings from cells in intact mouse islets ( N = 288 recordings) to investigate whether it is possible to reliably identify cell type (α, β or δ) based on their electrophysiological characteristics. We quantified 15 electrophysiological variables in each recorded cell. Individually, none of the variables could reliably distinguish the cell types. We therefore constructed a logistic regression model that included all quantified variables, to determine whether they could together identify cell type. The model identified cell type with 94% accuracy. This model was applied to a dataset of cells recorded from hyperglycaemic βV59M mice; it correctly identified cell type in all cells and was able to distinguish cells that co-expressed insulin and glucagon. Based on this revised functional identification, we were able to improve conductance-based models of the electrical activity in α-cells and generate a model of δ-cell electrical activity. These new models could faithfully emulate α- and δ-cell electrical activity recorded experimentally.

scholarly journals The pancreatic beta cell: an intricate relation between anatomical structure, the signalling mechanism of glucose-induced insulin secretion, the low antioxidative defence, the high vulnerability and sensitivity to diabetic stress

ChemTexts ◽  
2021 ◽  
Vol 7 (2) ◽  
Author(s):  
Sigurd Lenzen
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Islet Cell ◽  
Pancreatic Beta Cell ◽  
Cell Types ◽  
Antioxidative Defence ◽  
Islet Cell Types ◽  
Low Expression

AbstractThe biosynthesis of insulin takes place in the insulin-producing beta cells that are organized in the form of islets of Langerhans together with a few other islet cell types in the pancreas organ. The signal for glucose-induced insulin secretion is generated in two pathways in the mitochondrial metabolism of the pancreatic beta cells. These pathways are also known as the triggering pathway and the amplifying pathway. Glucokinase, the low-affinity glucose-phosphorylating enzyme in beta cell glycolysis acts as the signal-generating enzyme in this process. ATP ultimately generated is the crucial second messenger in this process. Insulin-producing pancreatic beta cells are badly protected against oxidative stress resulting in a particular vulnerability of this islet cell type due to low expression of H2O2-inactivating enzymes in various subcellular locations, specifically in the cytosol, mitochondria, peroxisomes and endoplasmic reticulum. This is in contrast to the glucagon-producing alpha cells and other islet cell types in the islets that are well equipped with these H2O2-inactivating enzymes. On the other hand the membranes of the pancreatic beta cells are well protected against lipid peroxidation and ferroptosis through high level expression of glutathione peroxidase 4 (GPx4) and this again is at variance from the situation in the non-beta cells of the islets with a low expression level of GPx4. The weak antioxidative defence equipment of the pancreatic beta cells, in particular in states of disease, is very dangerous because the resulting particular vulnerability endangers the functionality of the beta cells, making people prone to the development of a diabetic metabolic state.

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