scholarly journals Cavβ3 Regulates Ca2+-Signalling and Insulin Expression in Pancreatic β-Cells in a Cellautonomous Manner

Diabetes ◽  
2021 ◽  
pp. db210078
Author(s):  
Alexander Becker ◽  
Barbara Wardas ◽  
Houssein Salah ◽  
Maryam Amini ◽  
Claudia Fecher-Trost ◽  
...  
Keyword(s):  
Β Cells ◽  
Pancreatic Β Cells ◽  
Insulin Expression

scholarly journals Cx36 makes channels coupling human pancreatic β-cells, and correlates with insulin expression

2008 ◽  
Vol 18 (3) ◽  
pp. 428-439 ◽  
Author(s):  
Véronique Serre-Beinier ◽  
Domenico Bosco ◽  
Laurence Zulianello ◽  
Anne Charollais ◽  
Dorothée Caille ◽  
...  
Keyword(s):  
Β Cells ◽  
Pancreatic Β Cells ◽  
Insulin Expression

Pancreatic stellate cells reduce insulin expression and induce apoptosis in pancreatic β-cells

2013 ◽  
Vol 433 (3) ◽  
pp. 292-297 ◽  
Author(s):  
Kazuhiro Kikuta ◽  
Atsushi Masamune ◽  
Shin Hamada ◽  
Tetsuya Takikawa ◽  
Eriko Nakano ◽  
...  
Keyword(s):  
Stellate Cells ◽  
Pancreatic Stellate Cells ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Insulin Expression

scholarly journals Specific deletion of CDC42 in pancreatic β cells attenuates glucose-induced insulin expression and secretion in mice

2020 ◽  
Vol 518 ◽  
pp. 111004
Author(s):  
Xiang-Qin He ◽  
Ning Wang ◽  
Juan-Juan Zhao ◽  
Dan Wang ◽  
Cai-Ji Wang ◽  
...  
Keyword(s):  
Β Cells ◽  
Pancreatic Β Cells ◽  
Insulin Expression ◽  
Specific Deletion

Fatty acids induce amylin expression and secretion by pancreatic β-cells

2010 ◽  
Vol 298 (1) ◽  
pp. E99-E107 ◽  
Author(s):  
Dongfei Qi ◽  
Kun Cai ◽  
Oumei Wang ◽  
Zongmeng Li ◽  
Juan Chen ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Release ◽  
De Novo ◽  
Secretory Granules ◽  
Protein Synthesis Inhibitor ◽  
Transcriptional Level ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Min6 Cells ◽  
Insulin Expression

Amylin is the major component of pancreatic amyloid, which is implicated in the development of type 2 diabetes. It is costored with insulin in the secretory granules of pancreatic β-cells and cosecreted with insulin following stimulation with glucose. Here, we investigate the effect of fatty acids (FAs) on amylin expression and secretion by β-cells and explore the underlying mechanisms. Palmitate and oleate dose-dependently induced amylin mRNA accumulation in murine pancreatic β-cell line MIN6 and primary pancreatic islets. the inductive effect of FAs on amylin expression is independent of glucose concentration. FAs upregulated amylin expression at the transcriptional level, and FAs must be metabolized to induce amylin expression. FAs also significantly induced human amylin promoter activation. Pretreatment of MIN6 cells with Ca2+ chelator (EGTA, BAPTA-AM) PKC inhibitor Gö-6976 or protein synthesis inhibitor cycloheximide significantly inhibited FA-induced amylin mRNA expression. Transcription factors cAMP-responsive element-binding protein, pancreatic and duodenal homeobox factor-1, and peroxisome proliferator-activated receptor were not involved in FA-induced amylin expression. Palmitate and oleate both increased amylin and insulin release from MIN6 cells and stimulated amylin expression but had no effect on insulin expression. Mice refed with Intralipid had significantly higher levels of plasma FFA, amylin, and insulin than those refed with saline. These data demonstrate that FAs differently regulate amylin and insulin expression and induce both amylin and insulin release. Ca2+ and PKC signaling pathways and de novo-synthesized protein(s) were involved in FA-induced amylin expression. Induction of amylin production and release by FA may contribute to its biological functions under physiological conditions.

scholarly journals Cavβ3 regulates Ca2+-signalling and insulin expression in pancreatic β-cells in a cell-autonomous manner

2021 ◽  
Author(s):  
Alexander Becker ◽  
Barbara Wardas ◽  
Houssein Salah ◽  
Maryam Amini ◽  
Claudia Fecher‐Trost ◽  
...  
Keyword(s):  
Protein Profiling ◽  
Dependent Manner ◽  
Ip3 Receptor ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Concentration Dependent Manner ◽  
Insulin Expression ◽  
Low Concentrations ◽  
A Cell ◽  
Nitric Oxide Synthase 1

<p>Voltage-gated Ca<sup>2+</sup> (Cav) channels consist of a pore-forming Cavα1 subunit and auxiliary Cavα2-δ and Cavβ subunits. In fibroblasts, Cavβ3, independent of its role as a Cav subunit, reduces the sensitivity to low concentrations of inositol-1,4,5-trisphosphate (IP3). Similarly, Cavβ3 could affect cytosolic [Ca<sup>2+</sup>] in pancreatic β-cells. Here, we deleted the Cavβ3-encoding gene <i>Cacnb3</i> in insulin-secreting rat β-(Ins-1) cells using CRISPR/Cas9. These cells were used as controls to investigate the role of Cavβ3 on Ca<sup>2+</sup>-signalling, glucose-induced insulin secretion (GIIS), Cav-channel activity and gene expression in wild-type cells in which Cavβ3 and the IP3-receptor were co-immunoprecipitated. Transcript and protein profiling revealed significantly increased levels of insulin transcription factor Mafa, CaMKIV, neuroendocrine convertase1 (Pcsk1) and nitric oxide synthase-1 (NOS-1) in Cavβ3-KO cells. In the absence of Cavβ3, Cav-currents were not altered. In contrast, CREB activity, the amount of MAFA protein and GIIS, the extent of IP3-dependent Ca<sup>2+</sup> release and the frequency of Ca<sup>2+</sup>-oscillations were increased. These processes were decreased by the Cavβ3 protein in a concentration-dependent manner. Our study shows that Cavβ3 interacts with the IP3-receptor in isolated β-cells, controls IP3-dependent Ca<sup>2+</sup>-signalling independently of Cav channel functions, and thereby regulates insulin expression and its glucose-dependent release in a cell-autonomous manner.</p>

scholarly journals Cavβ3 regulates Ca2+-signalling and insulin expression in pancreatic β-cells in a cell-autonomous manner

2021 ◽  
Author(s):  
Alexander Becker ◽  
Barbara Wardas ◽  
Houssein Salah ◽  
Maryam Amini ◽  
Claudia Fecher‐Trost ◽  
...  
Keyword(s):  
Protein Profiling ◽  
Dependent Manner ◽  
Ip3 Receptor ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Concentration Dependent Manner ◽  
Insulin Expression ◽  
Low Concentrations ◽  
A Cell ◽  
Nitric Oxide Synthase 1

<p>Voltage-gated Ca<sup>2+</sup> (Cav) channels consist of a pore-forming Cavα1 subunit and auxiliary Cavα2-δ and Cavβ subunits. In fibroblasts, Cavβ3, independent of its role as a Cav subunit, reduces the sensitivity to low concentrations of inositol-1,4,5-trisphosphate (IP3). Similarly, Cavβ3 could affect cytosolic [Ca<sup>2+</sup>] in pancreatic β-cells. Here, we deleted the Cavβ3-encoding gene <i>Cacnb3</i> in insulin-secreting rat β-(Ins-1) cells using CRISPR/Cas9. These cells were used as controls to investigate the role of Cavβ3 on Ca<sup>2+</sup>-signalling, glucose-induced insulin secretion (GIIS), Cav-channel activity and gene expression in wild-type cells in which Cavβ3 and the IP3-receptor were co-immunoprecipitated. Transcript and protein profiling revealed significantly increased levels of insulin transcription factor Mafa, CaMKIV, neuroendocrine convertase1 (Pcsk1) and nitric oxide synthase-1 (NOS-1) in Cavβ3-KO cells. In the absence of Cavβ3, Cav-currents were not altered. In contrast, CREB activity, the amount of MAFA protein and GIIS, the extent of IP3-dependent Ca<sup>2+</sup> release and the frequency of Ca<sup>2+</sup>-oscillations were increased. These processes were decreased by the Cavβ3 protein in a concentration-dependent manner. Our study shows that Cavβ3 interacts with the IP3-receptor in isolated β-cells, controls IP3-dependent Ca<sup>2+</sup>-signalling independently of Cav channel functions, and thereby regulates insulin expression and its glucose-dependent release in a cell-autonomous manner.</p>

MICROCHEMICAL ASSAYS OF GLUCOSE AND GLUCOSE-6-PHOSPHATE IN MAMMALIAN PANCREATIC β-CELLS

1968 ◽  
Vol 59 (3) ◽  
pp. 479-486 ◽  
Author(s):  
Lars-Ake Idahl ◽  
Bo Hellman
Keyword(s):  
Glucose Level ◽  
Exocrine Pancreas ◽  
The Other ◽  
Wide Concentration Range ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Enzymatic Cycling ◽  
Glucose Diffusion ◽  
Significant Barrier ◽  
The Brain

ABSTRACT The combination of enzymatic cycling and fluorometry was used for measuring glucose and glucose-6-phosphate in pancreatic β-cells from obese-hyperglycaemic mice. The glucose level of the β-cells corresponded to that of serum over a wide concentration range. In the exocrine pancreas, on the other hand, a significant barrier to glucose diffusion across the cell membranes was demonstrated. During 5 min of ischaemia, the glucose level remained practically unchanged in the β-cells while it increased in the liver and decreased in the brain. The observation that the pancreatic β-cells are characterized by a relatively low ratio of glucose-6-phosphate to glucose may be attributed to the presence of a specific glucose-6-phosphatase.

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