Loss of GLUT2 glucose transporter expression in pancreatic beta cells from diabetic Chinese hamsters

1996 ◽  
Vol 428 (3) ◽  
Author(s):  
A. J�rns ◽  
M. Tiedge ◽  
S. Lenzen ◽  
E. Sickel
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Glucose Transporter ◽  
Chinese Hamsters ◽  
Diabetic Chinese Hamsters ◽  
Transporter Expression ◽  
Glut2 Glucose Transporter

scholarly journals Persistent glucose transporter expression on pancreatic beta cells from longstanding type 1 diabetic individuals

2011 ◽  
Vol 27 (8) ◽  
pp. 746-754 ◽  
Author(s):  
Ken T. Coppieters ◽  
Anna Wiberg ◽  
Natalie Amirian ◽  
Thomas W. Kay ◽  
Matthias G. von Herrath
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Glucose Transporter ◽  
Transporter Expression

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

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.

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.

scholarly journals Effects of Sclerocarya birrea Stem-Bark Extracts on Glucose Uptake, Insulin Synthesis and Expression of Selected Genes Involved in the Synthesis and Secretion of Insulin in Rat Insulinoma Pancreatic Beta Cells

2020 ◽  
Vol 32 (9) ◽  
pp. 2195-2202
Author(s):  
A.H. KGOPA ◽  
L.J. SHAI ◽  
M.A. MOGALE
Keyword(s):  
Glucose Uptake ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Glucose Transporter ◽  
Stem Bark ◽  
Hexane Extract ◽  
Insulin Synthesis ◽  
Sclerocarya Birrea ◽  
Glucose Transporter 2 ◽  
Rat Insulinoma

The present study reported the effects of Sclerocarya birrea stem-bark (SBSB) extracts on glucose uptake, insulin synthesis and the expression of glucose transporter 2 (GLUT2), glucokinase, pancreatic duodenal homeobox-1 (PDX-1), musculoaponeurotic fibrosarcoma oncogene homolog A (MafA) and pre-proinsulin genes in rat insulinoma (RIN)-m5F pancreatic beta cells. The amount of glucose takenup by RIN-m5F cells was measured using a glucose oxidase-based assay kit. Intracellular and secreted insulin were measured using an enzyme linked immunoassay kit. Pre-proinsulin gene expression was determined using the conventional polymerase chain reaction (PCR) technique, while the expressions of GLUT2, glucokinase, PDX-1 and MafA genes were evaluated using quantitative real-time PCR technique. Of the four SBSB extracts investigated in the study, only the SBSB hexane extract positively affected all the study variables in RIN-m5F cells compared with the DMSO control. Thus, the SBSB hexane extract contains phytochemicals capable of enhancing insulin synthesis partly through up-regulation of the expression of GLUT2, glucokinase, PDX-1, MafA and pre-proinsulin genes.

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