The Effect of Scaffold on the Morphology and Insulin Secretion of Islet Cells

2008 ◽  
pp. 157-162
Author(s):  
Takanori Kanayama ◽  
Hirofumi Mitsuishi ◽  
Satoshi Terada
Keyword(s):  
Insulin Secretion ◽  
Islet Cells

scholarly journals GRK2 contributes to glucose mediated calcium responses and insulin secretion in pancreatic islet cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jonathan Snyder ◽  
Atreju I Lackey ◽  
G. Schuyler Brown ◽  
Melisa Diaz ◽  
Tian Yuzhen ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Cell Model ◽  
Metabolic Phenotype ◽  
Atp Production ◽  
Pancreatic Islets Of Langerhans ◽  
Cardiac Mitochondrion ◽  
Pre Treatment ◽  
Insulin Responses

AbstractDiabetes is a metabolic syndrome rooted in impaired insulin and/or glucagon secretory responses within the pancreatic islets of Langerhans (islets). Insulin secretion is primarily regulated by two key factors: glucose-mediated ATP production and G-protein coupled receptors (GPCRs) signaling. GPCR kinase 2 (GRK2), a key regulator of GPCRs, is reported to be downregulated in the pancreas of spontaneously obesogenic and diabetogenic mice (ob/ob). Moreover, recent studies have shown that GRK2 non-canonically localizes to the cardiac mitochondrion, where it can contribute to glucose metabolism. Thus, islet GRK2 may impact insulin secretion through either mechanism. Utilizing Min6 cells, a pancreatic ß-cell model, we knocked down GRK2 and measured glucose-mediated intracellular calcium responses and insulin secretion. Silencing of GRK2 attenuated calcium responses, which were rescued by pertussis toxin pre-treatment, suggesting a Gαi/o-dependent mechanism. Pancreatic deletion of GRK2 in mice resulted in glucose intolerance with diminished insulin secretion. These differences were due to diminished insulin release rather than decreased insulin content or gross differences in islet architecture. Furthermore, a high fat diet feeding regimen exacerbated the metabolic phenotype in this model. These results suggest a new role for pancreatic islet GRK2 in glucose-mediated insulin responses that is relevant to type 2 diabetes disease progression.

scholarly journals A comparative study of amino acid consumption by rat islet cells and the clonal beta-cell line BRIN-BD11 - the functional significance of L-alanine

2003 ◽  
Vol 179 (3) ◽  
pp. 447-454 ◽  
Author(s):  
G Dixon ◽  
J Nolan ◽  
N McClenaghan ◽  
PR Flatt ◽  
P Newsholme
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Cell Line ◽  
Islet Cells ◽  
Beta Cell Line ◽  
Acid Consumption ◽  
Glutamine Consumption ◽  
Order Of Magnitude ◽  
Stimulus Secretion Coupling ◽  
Insulinotropic Effect

Evidence has been published that L -alanine may, under appropriate conditions, promote insulin secretion in normal rodent islets and various beta cell lines. Previous results utilising the clonal beta-cell line BRIN-BD11, demonstrated that alanine dramatically elevated insulin release by a mechanism requiring oxidative metabolism. We demonstrate in this paper that addition ofL -alanine had an insulinotropic effect in dispersed primary islet cells. Addition of D -glucose increasedL -alanine consumption in both BRIN-BD11 cells and primary islet cells.L -glutamine consumption in the BRIN-BD11 cell line and primary rat islets was also determined. The consumption rate was in line with that previously reported for cells of the immune system and other glutamine-utilising cells or tIssues. However,L -alanine consumption was at least an order of magnitude higher thanL -glutamine consumption. The metabolism ofL -alanine in the beta-cell may result in stimulation of insulin secretion via generation of metabolic stimulus secretion coupling factors such asL -glutamate.

scholarly journals Taurine supplementation: involvement of cholinergic/phospholipase C and protein kinase A pathways in potentiation of insulin secretion and Ca2+handling in mouse pancreatic islets

2010 ◽  
Vol 104 (8) ◽  
pp. 1148-1155 ◽  
Author(s):  
Rosane A. Ribeiro ◽  
Emerielle C. Vanzela ◽  
Camila A. M. Oliveira ◽  
Maria L. Bonfleur ◽  
Antonio C. Boschero ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Protein Kinase ◽  
Pancreatic Islets ◽  
Phospholipase C ◽  
Islet Cells ◽  
Taurine Supplementation ◽  
Adult Mice ◽  
Intracellular Ca ◽  
Mouse Pancreatic Islets ◽  
Methyl Xanthine

Taurine (TAU) supplementation increases insulin secretion in response to high glucose concentrations in rodent islets. This effect is probably due to an increase in Ca2+handling by the islet cells. Here, we investigated the possible involvement of the cholinergic/phospholipase C (PLC) and protein kinase (PK) A pathways in this process. Adult mice were fed with 2 % TAU in drinking water for 30 d. The mice were killed and pancreatic islets isolated by the collagenase method. Islets from TAU-supplemented mice showed higher insulin secretion in the presence of 8·3 mm-glucose, 100 μm-carbachol (Cch) and 1 mm-3-isobutyl-1-methyl-xanthine (IBMX), respectively. The increase in insulin secretion in response to Cch in TAU islets was accompanied by a higher intracellular Ca2+mobilisation and PLCβ2protein expression. The Ca2+uptake was higher in TAU islets in the presence of 8·3 mm-glucose, but similar when the islets were challenged by glucose plus IBMX. TAU islets also showed an increase in the expression of PKAα protein. This protein may play a role in cation accumulation, since the amount of Ca2+in these islets was significantly reduced by the PKA inhibitors:N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline sulfonamide (H89) and PK inhibitor-(6–22)-amide (PKI). In conclusion, TAU supplementation increases insulin secretion in response to glucose, favouring both influx and internal mobilisation of Ca2+, and these effects seem to involve the activation of both PLC–inositol-1,4,5-trisphosphate and cAMP–PKA pathways.

Dietary fatty acids modify insulin secretion of rat pancreatic islet cells in vitro

2002 ◽  
Vol 25 (5) ◽  
pp. 436-441 ◽  
Author(s):  
F. J. Tinahones ◽  
A. Pareja ◽  
F. J. Soriguer ◽  
J. M. Gómez-Zumaquero ◽  
F. Cardona ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Dietary Fatty Acids ◽  
Pancreatic Islet Cells ◽  
Rat Pancreatic Islet

An osmotic-sensitive taurine pool is localized in rat pancreatic islet cells containing glucagon and somatostatin

2001 ◽  
Vol 281 (6) ◽  
pp. E1275-E1285 ◽  
Author(s):  
J. Bustamante ◽  
M. V. T. Lobo ◽  
F. J. Alonso ◽  
N.-T. A. Mukala ◽  
E. Giné ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Islet Cells ◽  
Second Phase ◽  
Pancreatic Islet Cells ◽  
Taurine Release ◽  
Glucose Stimulation ◽  
Basal Release ◽  
Double Immunolabeling ◽  
Rat Pancreatic Islet ◽  
Phasic Release

Previous reports have dealt with the hypoglycemic properties of taurine and its effects on insulin secretion by adult and fetal isolated islets. We have studied the presence and cellular distribution of taurine in rat islets, the conditions to evoke its release, and its possible modulatory action on insulin secretion. We localized taurine by techniques of double immunolabeling in most glucagon-positive cells and in some somatostatin-positive cells, whereas insulin-positive cells were not labeled with the taurine antibody. Although high-glucose stimulation did not evoke any taurine release, a hyposmotic solution (17% osmolarity reduction) induced a specific phasic release of taurine and GABA (34 and 52% increase on their basal release rate). On the other hand, taurine (10 mmol/l) application slightly reduced the second phase of insulin secretion induced by glucose stimulation. In conclusion, taurine is highly concentrated in glucagon-containing cells of the islet periphery. It is not liberated by glucose stimulation but is strongly released under hyposmotic conditions. All of these data suggest that taurine plays an osmoregulatory role in α-cells.

Fluorescence-activated cell sorted rat islet cells and studies of the insulin secretory process

1996 ◽  
Vol 149 (1) ◽  
pp. 145-154 ◽  
Author(s):  
K Josefsen ◽  
J P Stenvang ◽  
H Kindmark ◽  
P-O Berggren ◽  
T Horn ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Beta Cells ◽  
Endocrine Cells ◽  
Islet Cells ◽  
Single Cells ◽  
Cell Types ◽  
Glucose Sensing ◽  
Secretory Process ◽  
Functional Coupling ◽  
Paracrine Interaction

Abstract Studies of individual cell types in the islets of Langerhans are complicated by the cells' functional coupling by gap junctions and paracrine interaction. Access to purified alpha and beta cells is therefore desirable. We present a simplified and optimized method for fluorescence-activated cell sorting of endocrine pancreatic rat islets. For dispersion of the islets, dispase was superior to trypsin, as the number of vital single cells was higher (1·1 ± 0·1 × 103 vs 0·6 ± 0·1 × 103/islet, P<0·05). The purity of the sorted cells was 96·7 ± 1·2% for the non-beta cells and 97·8 ± 0·6% for the beta cells (numbers in percentages of endocrine cells). In culture, isolated beta cells, non-beta cells and mixtures of beta and non-beta cells formed aggregates, but not at low temperature (4 °C) and not in medium with low serum content (2%). Finally, in pure beta cell aggregates, glucose stimulated changes in cytoplasmic free Ca2+ concentration although both glucose- and arginine-induced insulin secretion was much reduced. We conclude that alpha cells are necessary for insulin secretion but not for glucose sensing. Journal of Endocrinology (1996) 149, 145–154

scholarly journals Loss-of-Function Mutation of the Galanin Gene Is Associated with Perturbed Islet Function in Mice

Endocrinology ◽  
2004 ◽  
Vol 145 (7) ◽  
pp. 3190-3196 ◽  
Author(s):  
Bo Ahrén ◽  
Giovanni Pacini ◽  
David Wynick ◽  
Nils Wierup ◽  
Frank Sundler
Keyword(s):  
Insulin Secretion ◽  
Islet Cells ◽  
Insulin Response ◽  
Tolerance Test ◽  
Glucose Disposal ◽  
Islet Function ◽  
Loss Of Function ◽  
Euglycemic Hyperinsulinemic Clamp

Abstract The neuropeptide galanin is expressed in sympathetic nerve terminals that surround islet cells and inhibits insulin secretion. To explore its role for islet function, we studied mice with a loss-of-function mutation in the galanin gene [galanin knockout (KO) mice]. Intravenous 2-deoxy-glucose, which activates both the sympathetic and parasympathetic branches of the autonomic nervous system, caused an initial (1–5 min) inhibition of insulin secretion that was impaired in galanin KO mice (P = 0.027), followed by a subsequent stimulation of insulin secretion that was augmented in galanin KO mice (P &lt; 0.01). Similar effects were seen after chemical sympathectomy by 6-hydroxydopamine. In contrast, galanin KO mice had a reduced insulin response to glucose, both in vivo (P &lt; 0.001) and in isolated islets (P &lt; 0.001), and to arginine, both in vivo (P = 0.012) and in vitro (P = 0.018). During an iv glucose tolerance test, galanin KO mice had impaired glucose disposal (P = 0.005) due to a reduced insulin response (P &lt; 0.001) and a reduced insulin-independent glucose elimination (glucose effectiveness; P = 0.040). Insulin sensitivity, as judged by a euglycemic, hyperinsulinemic clamp technique, was slightly increased in galanin KO mice (P = 0.032). We conclude that 1) galanin may contribute to sympathetic influences inhibiting insulin secretion in mice, and 2) galanin KO mice have a reduced glucose-induced insulin secretion.

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