scholarly journals Chronic effect of fatty acids on insulin release is not through the alteration of glucose metabolism in a pancreatic beta-cell line (βHC9)

Diabetologia ◽  
1997 ◽  
Vol 40 (9) ◽  
pp. 1018-1027 ◽  
Author(s):  
Y. Liang ◽  
C. Buettger ◽  
D. K. Berner ◽  
F. M. Matschinsky
Keyword(s):  
Fatty Acids ◽  
Glucose Metabolism ◽  
Beta Cell ◽  
Cell Line ◽  
Insulin Release ◽  
Pancreatic Beta Cell ◽  
Chronic Effect ◽  
Beta Cell Line

scholarly journals Pancreatic beta cell line MIN6 exhibits characteristics of glucose metabolism and glucose-stimulated insulin secretion similar to those of normal islets

Diabetologia ◽  
1993 ◽  
Vol 36 (11) ◽  
pp. 1139-1145 ◽  
Author(s):  
H. Ishihara ◽  
T. Asano ◽  
K. Tsukuda ◽  
H. Katagiri ◽  
K. Inukai ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Beta Cell ◽  
Cell Line ◽  
Pancreatic Beta Cell ◽  
Beta Cell Line ◽  
Glucose Stimulated Insulin Secretion

Glucose metabolism and insulin release in mouse beta HC9 cells, as model for wild-type pancreatic beta-cells

1996 ◽  
Vol 270 (5) ◽  
pp. E846-E857 ◽  
Author(s):  
Y. Liang ◽  
G. Bai ◽  
N. Doliba ◽  
C. Buettger ◽  
L. Wang ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Beta Cell ◽  
Cell Line ◽  
Insulin Release ◽  
Cell Lines ◽  
Pancreatic Beta Cells ◽  
Pancreatic Beta Cell ◽  
Glucose Sensing ◽  
Cell Functions ◽  
Glucose Phosphorylation

Glucose metabolism and its relationship with glucose-induced insulin release were studied in beta HC9 and beta TC3 cells to identify and characterize key factors controlling the intermediary metabolism of glucose and glucose-induced insulin release. The beta HC9 cell line, derived from pancreatic islets with beta-cell hyperplasia, is characterized by a normal concentration-dependency curve for glucose-stimulated insulin release, whereas the beta TC3 cell line, derived from pancreatic beta-cell tumors, shows a marked leftward shift of this curve. Maximum velocity and the Michaelis-Menten constant of glucose uptake in beta HC9 and beta TC3 cells were similar, even though GLUT-2 expression in these two cell lines differed. In both cell lines, the kinetic characteristics of glucose usage, glucose oxidation, and glucose-induced oxygen consumption were similar to those of glucose phosphorylation, indicating that the kinetics of glucose metabolism from the glucose phosphorylation step in the cytosol to the mitochondrial process of oxidative phosphorylation are determined by the glucose-phosphorylating enzyme, that is, by glucokinase in beta HC9 cells and by hexokinase in beta TC3 cells. Thus beta HC9 cells provide an opportunity for the quantitative analysis of glucose metabolism, the associated generation of coupling factors, and other essential beta-cell functions involved in glucose sensing and insulin secretion.

Long-chain fatty acids inhibit acetyl-CoA carboxylase gene expression in the pancreatic beta-cell line INS-1

Diabetes ◽  
1997 ◽  
Vol 46 (3) ◽  
pp. 393-400 ◽  
Author(s):  
T. Brun ◽  
F. Assimacopoulos-Jeannet ◽  
B. E. Corkey ◽  
M. Prentki
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Beta Cell ◽  
Cell Line ◽  
Pancreatic Beta Cell ◽  
Long Chain Fatty Acids ◽  
Acetyl Coa Carboxylase ◽  
Acetyl Coa ◽  
Beta Cell Line ◽  
Long Chain

scholarly journals 13C NMR analysis reveals a link between L-glutamine metabolism, D-glucose metabolism and ?-glutamyl cycle activity in a clonal pancreatic beta-cell line

Diabetologia ◽  
2003 ◽  
Vol 46 (11) ◽  
pp. 1512-1521 ◽  
Author(s):  
L. Brennan ◽  
M. Corless ◽  
C. Hewage ◽  
J. P. G. Malthouse ◽  
N. H. McClenaghan ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Beta Cell ◽  
Cell Line ◽  
13C Nmr ◽  
Pancreatic Beta Cell ◽  
Glutamine Metabolism ◽  
Nmr Analysis ◽  
13C Nmr Analysis ◽  
Beta Cell Line

Long-term elevation of free fatty acids leads to delayed processing of proinsulin and prohormone convertases 2 and 3 in the pancreatic beta-cell line MIN6

Diabetes ◽  
1999 ◽  
Vol 48 (7) ◽  
pp. 1395-1401 ◽  
Author(s):  
H. Furukawa ◽  
R. J. Carroll ◽  
H. H. Swift ◽  
D. F. Steiner
Keyword(s):  
Fatty Acids ◽  
Beta Cell ◽  
Free Fatty Acids ◽  
Cell Line ◽  
Pancreatic Beta Cell ◽  
Prohormone Convertases ◽  
Beta Cell Line

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 Regulated expression and function of the GABAB receptor in human pancreatic beta cell line and islets

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Latif Rachdi ◽  
Alicia Maugein ◽  
Severine Pechberty ◽  
Mathieu Armanet ◽  
Juliette Hamroune ◽  
...  
Keyword(s):  
Beta Cell ◽  
Cell Line ◽  
Gabab Receptor ◽  
Pancreatic Beta Cell ◽  
Beta Cell Line ◽  
Regulated Expression ◽  
And Function

Functional analysis of a conditionally transformed pancreatic beta-cell line

Diabetes ◽  
1998 ◽  
Vol 47 (9) ◽  
pp. 1419-1425 ◽  
Author(s):  
N. Fleischer ◽  
C. Chen ◽  
M. Surana ◽  
M. Leiser ◽  
L. Rossetti ◽  
...  
Keyword(s):  
Functional Analysis ◽  
Beta Cell ◽  
Cell Line ◽  
Pancreatic Beta Cell ◽  
Beta Cell Line

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 Identification of genes regulated by glucose in a pancreatic beta-cell line by a new method for subtraction of mRNA

Diabetologia ◽  
1996 ◽  
Vol 39 (11) ◽  
pp. 1293-1298 ◽  
Author(s):  
E. Yamato ◽  
H. Ikegami ◽  
J.-I. Miyazaki ◽  
T. Ogihara
Keyword(s):  
Beta Cell ◽  
Cell Line ◽  
Pancreatic Beta Cell ◽  
New Method ◽  
Beta Cell Line
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