scholarly journals Human Beta Cells Produce and Release Serotonin to Inhibit Glucagon Secretion from Alpha Cells

Cell Reports ◽  
2016 ◽  
Vol 17 (12) ◽  
pp. 3281-3291 ◽  
Author(s):  
Joana Almaça ◽  
Judith Molina ◽  
Danusa Menegaz ◽  
Alexey N. Pronin ◽  
Alejandro Tamayo ◽  
...  
Keyword(s):  
Beta Cells ◽  
Glucagon Secretion ◽  
Alpha Cells ◽  
Human Beta Cells

Glucagonotropic and Glucagonostatic Effects of KATP Channel Closure and Potassium Depolarization

Endocrinology ◽  
2020 ◽  
Vol 162 (1) ◽  
Author(s):  
Eike Früh ◽  
Christin Elgert ◽  
Frank Eggert ◽  
Stephan Scherneck ◽  
Ingo Rustenbeck
Keyword(s):  
Insulin Secretion ◽  
Beta Cells ◽  
Katp Channel ◽  
Glucagon Secretion ◽  
Alpha Cells ◽  
High Potassium ◽  
Intrinsic Signal ◽  
Mouse Islets ◽  
Glucagon And Insulin

Abstract The role of depolarization in the inverse glucose-dependence of glucagon secretion was investigated by comparing the effects of KATP channel block and of high potassium. The secretion of glucagon and insulin by perifused mouse islets was simultaneously measured. Lowering glucose raised glucagon secretion before it decreased insulin secretion, suggesting an alpha cell–intrinsic signal recognition. Raising glucose affected glucagon and insulin secretion at the same time. However, depolarization by tolbutamide, gliclazide, or 15 mM KCl increased insulin secretion before the glucagon secretion receded. In contrast to the robust depolarizing effect of arginine and KCl (15 and 40 mM) on single alpha cells, tolbutamide was of variable efficacy. Only when applied before other depolarizing agents had tolbutamide a consistent depolarizing effect and regularly increased the cytosolic Ca2+ concentration. When tested on inside-out patches tolbutamide was as effective on alpha cells as on beta cells. In the presence of 1 µM clonidine, to separate insulinotropic from glucagonotropic effects, both 500 µM tolbutamide and 30 µM gliclazide increased glucagon secretion significantly, but transiently. The additional presence of 15 or 40 mM KCl in contrast led to a marked and lasting increase of the glucagon secretion. The glucagon secretion by SUR1 knockout islets was not increased by tolbutamide, whereas 40 mM KCl was of unchanged efficiency. In conclusion a strong and sustained depolarization is compatible with a marked and lasting glucagon secretion. KATP channel closure in alpha cells is less readily achieved than in beta cells, which may explain the moderate and transient glucagonotropic effect.

scholarly journals Abnormal regulation of glucagon secretion by human islet alpha cells in the absence of beta cells

EBioMedicine ◽  
2019 ◽  
Vol 50 ◽  
pp. 306-316 ◽  
Author(s):  
Wei Liu ◽  
Tatsuya Kin ◽  
Siuhong Ho ◽  
Craig Dorrell ◽  
Sean R. Campbell ◽  
...  
Keyword(s):  
Beta Cells ◽  
Glucagon Secretion ◽  
Human Islet ◽  
Alpha Cells

PS18 - 87. Transdifferentation of human beta-cells into alpha-cells

2011 ◽  
Vol 9 (3) ◽  
pp. 151-151
Author(s):  
H. Siebe Spijker ◽  
Mieke Mommaas-Kienhuis ◽  
Jos Onderwater ◽  
Aart van Apeldoorn ◽  
Marten Engelse ◽  
...  
Keyword(s):  
Beta Cells ◽  
Alpha Cells ◽  
Human Beta Cells

scholarly journals Hyperglycemia-Induced Proliferation of Adult Human Beta Cells Engrafted Into Spontaneously Diabetic Immunodeficient NOD-Rag1null IL2rγnull Ins2Akita Mice

Pancreas ◽  
2011 ◽  
Vol 40 (7) ◽  
pp. 1147-1149 ◽  
Author(s):  
Philip diIorio ◽  
Agata Jurczyk ◽  
Chaoxing Yang ◽  
Waldemar J. Racki ◽  
Michael A. Brehm ◽  
...  
Keyword(s):  
Beta Cells ◽  
Adult Human ◽  
Human Beta Cells

scholarly journals Bioluminescent reporter assay for monitoring ER stress in human beta cells

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Maria J. L. Kracht ◽  
Eelco J. P. de Koning ◽  
Rob C. Hoeben ◽  
Bart O. Roep ◽  
Arnaud Zaldumbide
Keyword(s):  
Er Stress ◽  
Beta Cells ◽  
Reporter Assay ◽  
Human Beta Cells

scholarly journals Cloning and quantitative determination of the human Ca 2+ /calmodulin-dependent protein kinase II (CaMK II) isoforms in human beta cells

Diabetologia ◽  
2000 ◽  
Vol 43 (4) ◽  
pp. 465-473 ◽  
Author(s):  
H. Rochlitz ◽  
A. Voigt ◽  
B. Lankat-Buttgereit ◽  
B. G�ke ◽  
H. Heimberg ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Quantitative Determination ◽  
Beta Cells ◽  
Dependent Protein Kinase ◽  
Protein Kinase Ii ◽  
Human Beta Cells ◽  
Dependent Protein

scholarly journals Mitochondria as a Target for Future Diabetes Treatments

2015 ◽  
Vol 3 (1) ◽  
pp. 45-50
Author(s):  
Franziska Thimm ◽  
Marten Szibor
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Life Support ◽  
Diabetes Management ◽  
Glucagon Secretion ◽  
Treatment Method ◽  
Serial Killer ◽  
Diabetic Patients ◽  
Insulin Resistant ◽  
Islet Transplants

Diabetes mellitus is rapidly becoming the world’s most dangerous serial killer. Type 1 diabetes (T1D) is a currently incurable autoimmune disease marked by progressive, and eventually exhaustive, destruction of the insulin-producing pancreatic beta cells. Type 2 diabetes (T2D) describes the combination of insulin resistance in peripheral tissue, insufficient insulin secretion from the pancreatic beta cells, and excessive glucagon secretion from the pancreatic alpha cells. T1D as well as severe cases of T2D are treated with insulin replacement, which can merely be considered as life support for the acute phases of the disease. Islet replacement of insulin-producing pancreatic beta cells represents a potential treatment method for both insulin-depleted diabetes (T1D) and insulin-resistant diabetes (T2D) and may shift diabetes management from life saving measures to a cure. One of the key challenges in islet transplants is the generation of reactive oxygen species (ROS) and the associated oxidative stress, which restricts graft longevity. A major leak of ROS takes place during oxidative phosphorylation at mitochondrial electron transport chain (ETC). Additionally, hyperglycemia-induced superoxide (O2•-) production has been linked to the development and progression of diabetic complications, both macrovascular and microvascular. Decreasing ROS in diabetic patients may prevent the incidence of long term diabetes complications. This review provides an overview of the role of mitochondria in diabetes, introducing them as a possible target for future treatment of diabetes.

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