Glucose modulates glucose transporter affinity, glucokinase activity, and secretory response in rat pancreatic beta-cells

Diabetes ◽  
1993 ◽  
Vol 42 (1) ◽  
pp. 199-205 ◽  
Author(s):  
F. Purrello ◽  
M. Buscema ◽  
A. M. Rabuazzo ◽  
V. Caltabiano ◽  
F. Forte ◽  
...  
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Glucose Transporter ◽  
Secretory Response

scholarly journals Diabetes-Resistant NOR Mice Are More Severely Affected by Streptozotocin Compared to the Diabetes-Prone NOD Mice: Correlations with Liver and Kidney GLUT2 Expressions

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
S. Kahraman ◽  
C. Aydin ◽  
G. O. Elpek ◽  
E. Dirice ◽  
A. D. Sanlioglu
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Glucose Transporter ◽  
Expression Profiles ◽  
Nod Mice ◽  
Underlying Mechanism ◽  
Expression Levels ◽  
Similar Dose ◽  
Liver And Kidney ◽  
Immunohistochemical Studies

Nonobese Diabetic (NOD) mice are susceptible strains for Type 1 diabetes development, and Nonobese Diabetes-Resistant (NOR) mice are defined as suitable controls for NOD mice in non-MHC-related research. Diabetes is often accelerated in NOD mice via Streptozotocin (STZ). STZ is taken inside cells via GLUT2 transmembrane carrier proteins, the major glucose transporter isoforms in pancreatic beta cells, liver, kidneys, and the small intestine. We observed severe adverse effects in NOR mice treated with STZ compared to NOD mice that were made diabetic with a similar dose. We suggested that the underlying mechanism could be differential GLUT2 expressions in pancreatic beta cells, yet immunofluorescent and immunohistochemical studies revealed similar GLUT2 expression levels. We also detected GLUT2 expression profiles in NOD and NOR hepatic and renal tissues by western blot analysis and observed considerably higher GLUT2 expression levels in liver and kidney tissues of NOR mice. Although beta cell GLUT2 expression levels are frequently evaluated as a marker predicting STZ sensitivity in animal models, we report here very different diabetic responses to STZ in two different animal strains, in spite of similar initial GLUT2 expressions in beta cells. Furthermore, use of NOR mice in STZ-mediated experimental diabetes settings should be considered accordingly.

N-glycosylation modulates the membrane sub-domain distribution and activity of glucose transporter 2 in pancreatic beta cells

2013 ◽  
Vol 434 (2) ◽  
pp. 346-351 ◽  
Author(s):  
Kazuaki Ohtsubo ◽  
Shinji Takamatsu ◽  
Congxiao Gao ◽  
Hiroaki Korekane ◽  
Tsutomu M. Kurosawa ◽  
...  
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Glucose Transporter ◽  
Glucose Transporter 2

Cell-to-cell contact dependence and junctional protein content are correlated with in vivo maturation of pancreatic beta cells

2012 ◽  
Vol 90 (7) ◽  
pp. 837-850 ◽  
Author(s):  
Junia Carolina Santos-Silva ◽  
Carolina Prado de França Carvalho ◽  
Ricardo Beltrame de Oliveira ◽  
Antonio Carlos Boschero ◽  
Carla Beatriz Collares-Buzato
Keyword(s):  
Protein Content ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Secretory Response ◽  
Cell Contact ◽  
Isolated Cells ◽  
Differential Distribution ◽  
Cell Contacts ◽  
Junctional Protein ◽  
Cell Cell

In this study, we investigated the cellular distribution of junctional proteins and the dependence on cell–cell contacts of pancreatic beta cells during animal development. Fetus and newborn rat islets, which display a relatively poor insulin secretory response to glucose, present an immature morphology and cytoarchitecture when compared with young and adult islets that are responsive to glucose. At the perinatal stage, beta cells display a low junctional content of neural cell adhesion molecule (N-CAM), α- and β-catenins, ZO-1, and F-actin, while a differential distribution of N-CAM and Pan-cadherin was seen in beta cells and nonbeta cells only from young and adult islets. In the absence of intercellular contacts, the glucose-stimulated insulin secretion was completely blocked in adult beta cells, but after reaggregation they partially reestablished the secretory response to glucose. By contrast, neonatal beta cells were poorly responsive to sugar, regardless of whether they were arranged as intact islets or as isolated cells. Interestingly, after 10 days of culturing, neonatal beta cells, known to display increased junctional protein content in vitro, became responsive to glucose and concomitantly dependent on cell–cell contacts. Therefore, our data suggest that the developmental acquisition of an adult-like insulin secretory pattern is paralleled by a dependence on direct cell–cell interactions.

GLUT2 (SLC2A2) is not the principal glucose transporter in human pancreatic beta cells: Implications for understanding genetic association signals at this locus

2011 ◽  
Vol 104 (4) ◽  
pp. 648-653 ◽  
Author(s):  
Laura J. McCulloch ◽  
Martijn van de Bunt ◽  
Matthias Braun ◽  
Keith N. Frayn ◽  
Anne Clark ◽  
...  
Keyword(s):  
Beta Cells ◽  
Genetic Association ◽  
Pancreatic Beta Cells ◽  
Glucose Transporter

scholarly journals Gangliosides modulate insulin secretion by pancreatic beta cells under glucose stress

Glycobiology ◽  
2020 ◽  
Vol 30 (9) ◽  
pp. 722-734 ◽  
Author(s):  
Richard Jennemann ◽  
Sylvia Kaden ◽  
Martina Volz ◽  
Viola Nordström ◽  
Silke Herzer ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Uptake ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Glucose Transporter ◽  
Specific Model ◽  
Downstream Signaling ◽  
Glucose Levels ◽  
Glucose Transporter 2 ◽  
Lower Glucose

Abstract In pancreatic beta cells, the entry of glucose and downstream signaling for insulin release is regulated by the glucose transporter 2 (Glut2) in rodents. Dysfunction of the insulin-signaling cascade may lead to diabetes mellitus. Gangliosides, sialic acid-containing glycosphingolipids (GSLs), have been reported to modulate the function of several membrane proteins.Murine islets express predominantly sialylated GSLs, particularly the simple gangliosides GM3 and GD3 having a potential modulatory role in Glut2 activity. Conditional, tamoxifen-inducible gene targeting in pancreatic islets has now shown that mice lacking the glucosylceramide synthase (Ugcg), which represents the rate-limiting enzyme in GSL biosynthesis, displayed impaired glucose uptake and showed reduced insulin secretion. Consequently, mice with pancreatic GSL deficiency had higher blood glucose levels than respective controls after intraperitoneal glucose application. High-fat diet feeding enhanced this effect. GSL-deficient islets did not show apoptosis or ER stress and displayed a normal ultrastructure. Their insulin content, size and number were similar as in control islets. Isolated beta cells from GM3 synthase null mice unable to synthesize GM3 and GD3 also showed lower glucose uptake than respective control cells, corroborating the results obtained from the cell-specific model. We conclude that in particular the negatively charged gangliosides GM3 and GD3 of beta cells positively influence Glut2 function to adequately respond to high glucose loads.

Glucolipotoxicity promotes the capacity of the glycerolipid/NEFA cycle supporting the secretory response of pancreatic beta cells

Diabetologia ◽  
2022 ◽  
Author(s):  
Lucie Oberhauser ◽  
Cecilia Jiménez-Sánchez ◽  
Jesper Grud Skat Madsen ◽  
Dominique Duhamel ◽  
Susanne Mandrup ◽  
...  
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Secretory Response

Mice lacking the homeodomain transcription factor Nkx2.2 have diabetes due to arrested differentiation of pancreatic beta cells

Development ◽  
1998 ◽  
Vol 125 (12) ◽  
pp. 2213-2221 ◽  
Author(s):  
L. Sussel ◽  
J. Kalamaras ◽  
D.J. Hartigan-O'Connor ◽  
J.J. Meneses ◽  
R.A. Pedersen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Beta Cell ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Glucose Transporter ◽  
Large Population ◽  
Islet Amyloid ◽  
Cell Markers ◽  
Glucose Transporter 2 ◽  
Alpha Beta

The endocrine pancreas is organized into clusters of cells called islets of Langerhans comprising four well-defined cell types: alpha beta, delta and PP cells. While recent genetic studies indicate that islet development depends on the function of an integrated network of transcription factors, the specific roles of these factors in early cell-type specification and differentiation remain elusive. Nkx2.2 is a member of the mammalian NK2 homeobox transcription factor family that is expressed in the ventral CNS and the pancreas. Within the pancreas, we demonstrate that Nkx2.2 is expressed in alpha, beta and PP cells, but not in delta cells. In addition, we show that mice homozygous for a null mutation of Nkx2.2 develop severe hyperglycemia and die shortly after birth. Immunohistochemical analysis reveals that the mutant embryos lack insulin-producing beta cells and have fewer glucagon-producing alpha cells and PP cells. Remarkably, in the mutants there remains a large population of islet cells that do not produce any of the four endocrine hormones. These cells express some beta cell markers, such as islet amyloid polypeptide and Pdx1, but lack other definitive beta cell markers including glucose transporter 2 and Nkx6.1. We propose that Nkx2.2 is required for the final differentiation of pancreatic beta cells, and in its absence, beta cells are trapped in an incompletely differentiated state.

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