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Article ; Online: The Role of α-Cells in Islet Function and Glucose Homeostasis in Health and Type 2 Diabetes.

Gilon, Patrick

2020 Volume 432, Issue 5, Page(s) 1367–1394

Abstract: Pancreatic α-cells are the major source of glucagon, a hormone that counteracts the hypoglycemic action of insulin and strongly contributes to the correction of acute hypoglycemia. The mechanisms by which glucose controls glucagon secretion are hotly ... ...

Abstract	Pancreatic α-cells are the major source of glucagon, a hormone that counteracts the hypoglycemic action of insulin and strongly contributes to the correction of acute hypoglycemia. The mechanisms by which glucose controls glucagon secretion are hotly debated, and it is still unclear to what extent this control results from a direct action of glucose on α-cells or is indirectly mediated by β- and/or δ-cells. Besides its hyperglycemic action, glucagon has many other effects, in particular on lipid and amino acid metabolism. Counterintuitively, glucagon seems also required for an optimal insulin secretion in response to glucose by acting on its cognate receptor and, even more importantly, on GLP-1 receptors. Patients with diabetes mellitus display two main alterations of glucagon secretion: a relative hyperglucagonemia that aggravates hyperglycemia, and an impaired glucagon response to hypoglycemia. Under metabolic stress states, such as diabetes, pancreatic α-cells also secrete GLP-1, a glucose-lowering hormone, whereas the gut can produce glucagon. The contribution of extrapancreatic glucagon to the abnormal glucose homeostasis is unclear. Here, I review the possible mechanisms of control of glucagon secretion and the role of α-cells on islet function in healthy state. I discuss the possible causes of the abnormal glucagonemia in diabetes, with particular emphasis on type 2 diabetes, and I briefly comment the current antidiabetic therapies affecting α-cells.
MeSH term(s)	Animals ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/therapy ; Glucagon/metabolism ; Glucagon-Like Peptide 1/metabolism ; Glucagon-Like Peptide-1 Receptor/metabolism ; Glucagon-Secreting Cells/metabolism ; Glucose/metabolism ; Humans ; Hypoglycemia/physiopathology ; Hypoglycemia/therapy ; Insulin/metabolism
Chemical Substances	Glucagon-Like Peptide-1 Receptor ; Insulin ; Glucagon-Like Peptide 1 (89750-14-1) ; Glucagon (9007-92-5) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2020-01-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80229-3
ISSN	1089-8638 ; 0022-2836
ISSN (online)	1089-8638
ISSN	0022-2836
DOI	10.1016/j.jmb.2020.01.004
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Article ; Online: 3D evaluation of the extracellular matrix of hypoxic pancreatic islets using light sheet fluorescence microscopy.

Ramirez, Matias / Bastien, Estelle / Chae, Heeyoung / Gianello, Pierre / Gilon, Patrick / Bouzin, Caroline

Islets

2024 Volume 16, Issue 1, Page(s) 2298518

Abstract: Pancreatic islet transplantation is a promising treatment for type 1 diabetes, but the survival and function of transplanted islets are hindered by the loss of extracellular matrix (ECM) during islet isolation and by low oxygenation upon implantation. ... ...

Abstract	Pancreatic islet transplantation is a promising treatment for type 1 diabetes, but the survival and function of transplanted islets are hindered by the loss of extracellular matrix (ECM) during islet isolation and by low oxygenation upon implantation. This study aimed to evaluate the impact of hypoxia on ECM using a cutting-edge imaging approach based on tissue clearing and 3D microscopy. Human and rat islets were cultured under normoxic (O
MeSH term(s)	Humans ; Animals ; Rats ; Microscopy, Fluorescence ; Islets of Langerhans ; Extracellular Matrix ; Hypoxia ; Extracellular Matrix Proteins ; Cadherins
Chemical Substances	Extracellular Matrix Proteins ; Cadherins
Language	English
Publishing date	2024-01-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	2589489-4
ISSN	1938-2022 ; 1938-2022
ISSN (online)	1938-2022
ISSN	1938-2022
DOI	10.1080/19382014.2023.2298518
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Article ; Online: Cocaine- and amphetamine-regulated transcript: a novel regulator of energy homeostasis expressed in a subpopulation of pancreatic islet cells.

Gilon, Patrick

Diabetologia

2016 Volume 59, Issue 9, Page(s) 1855–1859

Abstract: Type 2 diabetes is characterised by chronic hyperglycaemia and its incidence is highly increased by exaggerated food consumption. It results from a lack of insulin action/production, but growing evidence suggests that it might also involve ... ...

Abstract	Type 2 diabetes is characterised by chronic hyperglycaemia and its incidence is highly increased by exaggerated food consumption. It results from a lack of insulin action/production, but growing evidence suggests that it might also involve hyperglucagonaemia and impaired control of glucose homeostasis by the brain. In recent years, the cocaine and amphetamine-regulated transcript (CART) peptides have generated a lot of interest in the battle against obesity because, via the brain, they exert anorexic effects and they increase energy expenditure. They are also localised, outside the brain, in discrete regions of the body and play a hormonal role in controlling various functions. In this issue of Diabetologia, the Wierup group (doi: 10.1007/s00125-016-4020-6 ) shows that CART peptides are expressed heterogeneously in islet cells of various species, including humans, and that their expression is upregulated in diabetes. The authors also shine a spotlight on some interesting effects of CART peptides on islet function, including stimulation of insulin secretion and inhibition of glucagon release. CART peptides would thus be at the centre of a cooperation between the brain and the endocrine pancreas to control glucose homeostasis. Although the mechanisms of action of CART peptides remain enigmatic because no specific receptor for these peptides has so far been discovered, their potential therapeutic use is evident and represents a new challenge for future research.
MeSH term(s)	Animals ; Brain/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Glucagon/metabolism ; Homeostasis/genetics ; Homeostasis/physiology ; Humans ; Hyperglycemia/metabolism ; Insulin/metabolism ; Islets of Langerhans/metabolism ; Nerve Tissue Proteins/metabolism
Chemical Substances	Insulin ; Nerve Tissue Proteins ; cocaine- and amphetamine-regulated transcript protein ; Glucagon (9007-92-5)
Language	English
Publishing date	2016-09
Publishing country	Germany
Document type	Editorial
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-016-4052-y
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Article ; Online: Glucose inhibits glucagon secretion by decreasing [Ca

Singh, Bilal / Khattab, Firas / Gilon, Patrick

Molecular metabolism

2022 Volume 61, Page(s) 101495

Abstract: Objective: The mechanisms by which glucose stimulates insulin secretion from β-cells are well established and involve inhibition of ATP-sensitive K: Methods: We tested the effect of a decrease or an increase of glucose concentration (Gx, with x = ... ...

Abstract	Objective: The mechanisms by which glucose stimulates insulin secretion from β-cells are well established and involve inhibition of ATP-sensitive K Methods: We tested the effect of a decrease or an increase of glucose concentration (Gx, with x = concentration in mM) on α-cell [Ca Results: Blockade of K Conclusions: We propose a model according to which glucose controls α-cell [Ca
MeSH term(s)	Adenosine Triphosphate ; Animals ; Calcium/metabolism ; Cations, Divalent/metabolism ; Exocytosis/physiology ; Glucagon/biosynthesis ; Glucagon/metabolism ; Glucagon-Secreting Cells/metabolism ; Glucose/analysis ; Glucose/metabolism ; KATP Channels/metabolism ; Mice ; Somatostatin/metabolism
Chemical Substances	Cations, Divalent ; KATP Channels ; Somatostatin (51110-01-1) ; Adenosine Triphosphate (8L70Q75FXE) ; Glucagon (9007-92-5) ; Glucose (IY9XDZ35W2) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-04-11
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2022.101495
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Article ; Online: Corrigendum to "Inter-domain tagging implicates caveolin-1 in insulin receptor trafficking and Erk signaling bias in pancreatic beta-cells" [Mol Metab 2016 May; 5 (5): 366-378].

Boothe, Tobias / Lim, Gareth E / Cen, Haoning / Skovsø, Søs / Piske, Micah / Li, Shu Nan / Nabi, Ivan R / Gilon, Patrick / Johnson, James D

Molecular metabolism

2024 Volume 83, Page(s) 101935

Language	English
Publishing date	2024-04-08
Publishing country	Germany
Document type	Published Erratum
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2024.101935
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Article ; Online: Glucose inhibits glucagon secretion by decreasing [Ca2+]c and by reducing the efficacy of Ca2+ on exocytosis via somatostatin-dependent and independent mechanisms

Bilal Singh / Firas Khattab / Patrick Gilon

Molecular Metabolism, Vol 61, Iss , Pp 101495- (2022)

2022

Abstract: Objective: The mechanisms by which glucose stimulates insulin secretion from β-cells are well established and involve inhibition of ATP-sensitive K+ (KATP) channels, followed by a rise in [Ca2+]c that triggers exocytosis. However, the mechanisms by which ...

Abstract	Objective: The mechanisms by which glucose stimulates insulin secretion from β-cells are well established and involve inhibition of ATP-sensitive K+ (KATP) channels, followed by a rise in [Ca2+]c that triggers exocytosis. However, the mechanisms by which glucose controls glucagon release from α-cells are much less known. In particular, it is debated whether the sugar controls glucagon secretion by changing α-cell [Ca2+]c, and whether KATP channels or paracrine factors are involved. The present study addresses these issues. Methods: We tested the effect of a decrease or an increase of glucose concentration (Gx, with x = concentration in mM) on α-cell [Ca2+]c and glucagon secretion. α-cell [Ca2+]c was monitored using GluCreGCaMP6f mice expressing the Ca2+-sensitive fluorescent protein, GCaMP6f, specifically in α-cells. [Ca2+]c was compared between dispersed α-cells and α-cells within islets to evaluate the potential contribution of an indirect effect of glucose. The same protocols were used for experiments of glucagon secretion from whole islets and [Ca2+]c measurements to test if changes in glucagon release mirror those in α-cell [Ca2+]c. Results: Blockade of KATP channels by sulfonylureas (tolbutamide 100 μM or gliclazide 25 μM) strongly increased [Ca2+]c in both dispersed α-cells and α-cells within islets. By contrast, glucose had no effect on [Ca2+]c in dispersed α-cells, whereas it affected it in α-cells within islets. The effect of glucose was however different in islets expressing (Sst+/+) or not somatostatin (SST) (Sst−/−). Decreasing glucose concentration from G7 to G1 modestly increased α-cell [Ca2+]c, but to a slightly larger extent in Sst+/+ islets than in Sst−/− islets. This G1-induced [Ca2+]c rise was also observed in the continuous presence of sulfonylureas in both Sst+/+ and Sst−/− islets. Increasing glucose concentration from G7 to G20 did not affect α-cell [Ca2+]c in Sst+/+ islets which remained low, whereas it strongly increased it in Sst−/− islets. The observations that this increase was seen ...
Keywords	Pancreatic islets ; KATP channels ; Ca2+ ; Glucagon ; Somatostatin ; Internal medicine ; RC31-1245
Subject code	570
Language	English
Publishing date	2022-07-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: ER stress increases expression of intracellular calcium channel RyR1 to modify Ca

Zhang, Irina X / Herrmann, Andrea / Leon, Juan / Jeyarajan, Sivakumar / Arunagiri, Anoop / Arvan, Peter / Gilon, Patrick / Satin, Leslie S

The Journal of biological chemistry

2023 Volume 299, Issue 8, Page(s) 105065

Abstract: Pancreatic beta cells maintain glucose homeostasis by secreting pulses of insulin in response to a rise in plasma glucose. Pulsatile insulin secretion occurs as a result of glucose-induced oscillations in beta-cell cytosolic ... ...

Abstract	Pancreatic beta cells maintain glucose homeostasis by secreting pulses of insulin in response to a rise in plasma glucose. Pulsatile insulin secretion occurs as a result of glucose-induced oscillations in beta-cell cytosolic Ca
MeSH term(s)	Animals ; Mice ; Apoptosis ; Calcium Signaling ; Diabetes Mellitus, Type 2/metabolism ; Endoplasmic Reticulum Stress ; Glucose/metabolism ; Homeostasis ; Insulin-Secreting Cells/metabolism ; Ryanodine Receptor Calcium Release Channel/genetics ; Ryanodine Receptor Calcium Release Channel/metabolism ; Tunicamycin ; Rats ; Cell Line
Chemical Substances	Glucose (IY9XDZ35W2) ; ryanodine receptor 1, mouse ; Ryanodine Receptor Calcium Release Channel ; Tunicamycin (11089-65-9)
Language	English
Publishing date	2023-07-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2023.105065
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Article ; Online: GLP-1 and GIP receptors signal through distinct β-arrestin 2-dependent pathways to regulate pancreatic β cell function.

Zaïmia, Nour / Obeid, Joelle / Varrault, Annie / Sabatier, Julia / Broca, Christophe / Gilon, Patrick / Costes, Safia / Bertrand, Gyslaine / Ravier, Magalie A

Cell reports

2023 Volume 42, Issue 11, Page(s) 113326

Abstract: Glucagon-like peptide 1 (GLP-1R) and glucose-dependent insulinotropic polypeptide (GIPR) receptors are G-protein-coupled receptors involved in glucose homeostasis. Diabetogenic conditions decrease β-arrestin 2 (ARRB2) levels in human islets. In mouse β ... ...

Abstract	Glucagon-like peptide 1 (GLP-1R) and glucose-dependent insulinotropic polypeptide (GIPR) receptors are G-protein-coupled receptors involved in glucose homeostasis. Diabetogenic conditions decrease β-arrestin 2 (ARRB2) levels in human islets. In mouse β cells, ARRB2 dampens insulin secretion by partially uncoupling cyclic AMP (cAMP)/protein kinase A (PKA) signaling at physiological doses of GLP-1, whereas at pharmacological doses, the activation of extracellular signal-related kinase (ERK)/cAMP-responsive element-binding protein (CREB) requires ARRB2. In contrast, GIP-potentiated insulin secretion needs ARRB2 in mouse and human islets. The GIPR-ARRB2 axis is not involved in cAMP/PKA or ERK signaling but does mediate GIP-induced F-actin depolymerization. Finally, the dual GLP-1/GIP agonist tirzepatide does not require ARRB2 for the potentiation of insulin secretion. Thus, ARRB2 plays distinct roles in regulating GLP-1R and GIPR signaling, and we highlight (1) its role in the physiological context and the possible functional consequences of its decreased expression in pathological situations such as diabetes and (2) the importance of assessing the signaling pathways engaged by the agonists (biased/dual) for therapeutic purposes.
MeSH term(s)	Mice ; Humans ; Animals ; Insulin-Secreting Cells/metabolism ; Glucagon-Like Peptide 1/metabolism ; Insulin/metabolism ; beta-Arrestin 2/metabolism ; beta-Arrestin 1/metabolism ; Glucose/metabolism
Chemical Substances	Glucagon-Like Peptide 1 (89750-14-1) ; Insulin ; beta-Arrestin 2 ; beta-Arrestin 1 ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-10-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.113326
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Article: Can Tea Extracts Exert a Protective Effect Against Diabetes by Reducing Oxidative Stress and Decreasing Glucotoxicity in Pancreatic β-Cells?

Chae, Heeyoung / Gilon, Patrick

Diabetes & metabolism journal

2015 Volume 39, Issue 1, Page(s) 27–30

Language	English
Publishing date	2015-02
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2602402-0
ISSN	2233-6087 ; 2233-6079
ISSN (online)	2233-6087
ISSN	2233-6079
DOI	10.4093/dmj.2015.39.1.27
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Article ; Online: K

Singh, Bilal / Khattab, Firas / Chae, Heeyoung / Desmet, Lieven / Herrera, Pedro L / Gilon, Patrick

Molecular metabolism

2021 Volume 53, Page(s) 101268

Abstract: Objective: Glucagon is secreted by pancreatic α-cells in response to hypoglycemia and its hyperglycemic effect helps to restore normal blood glucose. Insulin and somatostatin (SST) secretions from β- and δ-cells, respectively, are stimulated by glucose ... ...

Abstract	Objective: Glucagon is secreted by pancreatic α-cells in response to hypoglycemia and its hyperglycemic effect helps to restore normal blood glucose. Insulin and somatostatin (SST) secretions from β- and δ-cells, respectively, are stimulated by glucose by mechanisms involving an inhibition of their ATP-sensitive K Methods: Using a transgenic mouse model expressing the Ca Results: Application of the sulfonylureas, tolbutamide, or gliclazide, to a medium containing 1 mM or 15 mM glucose increased [Ca Conclusions: Sulfonylureas exert two opposite actions on α-cells: a direct stimulation as in β-cells and an indirect inhibition by SST. This suggests that any alteration of SST paracrine influence, as described in diabetes, will modify the effect of sulfonylureas on glucagon release. In addition, we suggest that δ-cells inhibit α-cells more efficiently than β-cells.
MeSH term(s)	Animals ; Calcium/metabolism ; Gliclazide/chemistry ; Gliclazide/pharmacology ; Glucagon/metabolism ; Glucagon-Secreting Cells/drug effects ; Glucagon-Secreting Cells/metabolism ; KATP Channels/antagonists & inhibitors ; KATP Channels/metabolism ; Mice ; Mice, Knockout ; Mice, Transgenic ; Potassium Channel Blockers/chemistry ; Potassium Channel Blockers/pharmacology ; Somatostatin/chemistry ; Somatostatin/pharmacology ; Tolbutamide/chemistry ; Tolbutamide/pharmacology
Chemical Substances	KATP Channels ; Potassium Channel Blockers ; Somatostatin (51110-01-1) ; Glucagon (9007-92-5) ; Tolbutamide (982XCM1FOI) ; Gliclazide (G4PX8C4HKV) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-06-09
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2021.101268
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