Pigment epithelium-derived factor (PEDF) regulates metabolism and insulin secretion from a clonal rat pancreatic beta cell line BRIN-BD11 and mouse islets

2016 ◽  
Vol 426 ◽  
pp. 50-60 ◽  
Author(s):  
Younan Chen ◽  
Rodrigo Carlessi ◽  
Nikita Walz ◽  
Vinicius Fernandes Cruzat ◽  
Kevin Keane ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Cell Line ◽  
Pigment Epithelium ◽  
Pancreatic Beta Cell ◽  
Pigment Epithelium Derived Factor ◽  
Beta Cell Line ◽  
Mouse Islets

The betaHC-9 pancreatic beta-cell line preserves the characteristics of progenitor mouse islets

Diabetes ◽  
1996 ◽  
Vol 45 (12) ◽  
pp. 1766-1773 ◽  
Author(s):  
M. Noda ◽  
M. Komatsu ◽  
G. W. Sharp
Keyword(s):  
Beta Cell ◽  
Cell Line ◽  
Pancreatic Beta Cell ◽  
Beta Cell Line ◽  
Mouse Islets

scholarly journals High dose of histone deacetylase inhibitors affects insulin secretory mechanism of pancreatic beta cell line

2018 ◽  
Vol 52 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Eiji Yamato
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Cell Line ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Pancreatic Beta Cell ◽  
High Dose ◽  
Min6 Cells ◽  
Beta Cell Line ◽  
High Doses

Abstract Objective. Histone deacytylase inhibitors (HDACis) inhibit the deacetylation of the lysine residue of proteins, including histones, and regulate the transcription of a variety of genes. Recently, HDACis have been used clinically as anti-cancer drugs and possible anti-diabetic drugs. Even though HDACis have been proven to protect the cytokine-induced damage of pancreatic beta cells, evidence also shows that high doses of HDACis are cytotoxic. In the present study, we, therefore, investigated the eff ect of HDACis on insulin secretion in a pancreatic beta cell line. Methods. Pancreatic beta cells MIN6 were treated with selected HDACis (trichostatin A, TSA; valproic acid, VPA; and sodium butyrate, NaB) in medium supplemented with 25 mM glucose and 13% heat-inactivated fetal bovine serum (FBS) for indicated time intervals. Protein expression of Pdx1 and Mafa in MIN6 cells was demonstrated by immunohistochemistry and immunocytochemistry, expression of Pdx1 and Mafa genes was measured by quantitative RT-PCR method. Insulin release from MIN6 cells and insulin cell content were estimated by ELISA kit. Superoxide production in MIN6 cells was measured using a Total ROS/Superoxide Detection System. Results. TSA, VPA, and NaB inhibited the expression of Pdx1 and Mafa genes and their products. TSA treatment led to beta cell malfunction, characterized by enhanced insulin secretion at 3 and 9 mM glucose, but impaired insulin secretion at 15 and 25 mM glucose. Th us, TSA induced dysregulation of the insulin secretion mechanism. TSA also enhanced reactive oxygen species production in pancreatic beta cells. Conclusions. Our results showed that HDACis caused failure to suppress insulin secretion at low glucose concentrations and enhance insulin secretion at high glucose concentrations. In other words, when these HDACis are used clinically, high doses of HDACis may cause hypoglycemia in the fasting state and hyperglycemia in the fed state. When using HDACis, physicians should, therefore, be aware of the capacity of these drugs to modulate the insulin secretory capacity of pancreatic beta cells.

scholarly journals Mitochondrial DNA Is Required for Regulation of Glucose-stimulated Insulin Secretion in a Mouse Pancreatic Beta Cell Line, MIN6

1996 ◽  
Vol 271 (42) ◽  
pp. 26194-26199 ◽  
Author(s):  
Aki Soejima ◽  
Kimiko Inoue ◽  
Daisaku Takai ◽  
Motohisa Kaneko ◽  
Hisamitsu Ishihara ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Insulin Secretion ◽  
Beta Cell ◽  
Cell Line ◽  
Pancreatic Beta Cell ◽  
Beta Cell Line ◽  
Glucose Stimulated Insulin Secretion

scholarly journals Sfrp5 increases glucose-stimulated insulin secretion in the rat pancreatic beta cell line INS-1E

PLoS ONE ◽  
2019 ◽  
Vol 14 (3) ◽  
pp. e0213650 ◽  
Author(s):  
Maren Carstensen-Kirberg ◽  
Karin Röhrig ◽  
Corinna Niersmann ◽  
D. Margriet Ouwens ◽  
Bengt F. Belgardt ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Cell Line ◽  
Pancreatic Beta Cell ◽  
Beta Cell Line ◽  
Glucose Stimulated Insulin Secretion

scholarly journals Effects of High Glucose Levels and Glycated Serum on GIP Responsiveness in the Pancreatic Beta Cell Line HIT-T15

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Alessandra Puddu ◽  
Roberta Sanguineti ◽  
Fabrizio Montecucco ◽  
Giorgio Luciano Viviani
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Cell Line ◽  
High Glucose ◽  
Intracellular Signaling ◽  
Pancreatic Beta Cells ◽  
Pancreatic Beta Cell ◽  
Diabetic Patients ◽  
Glucose Levels ◽  
Beta Cell Line

Glucose-dependent insulinotropic peptide (GIP) is an incretin hormone produced in the gastrointestinal tract that stimulates glucose dependent insulin secretion. Impaired incretin response has been documented in diabetic patients and was mainly related to the inability of the pancreatic beta cells to secrete insulin in response to GIP. Advanced Glycation End Products (AGEs) have been shown to play an important role in pancreatic beta cell dysfunction. The aim of this study is to investigate whether the exposure to AGEs can induce GIP resistance in the pancreatic beta cell line HIT-T15. Cells were cultured for 5 days in low (CTR) or high glucose (HG) concentration in the presence of AGEs (GS) to evaluate the expression of GIP receptor (GIPR), the intracellular signaling activated by GIP, and secretion of insulin in response to GIP. The results showed that incubation with GS alone altered intracellular GIP signaling and decreased insulin secretion as compared to CTR. GS in combination with HG reduced the expression of GIPR and PI3K and abrogated GIP-induced AKT phosphorylation and GIP-stimulated insulin secretion. In conclusion, we showed that treatment with GS is associated with the loss of the insulinotropic effect of GIP in hyperglycemic conditions.

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