Generation of a Novel Mouse Model to Study Pancreatic Beta-Cell Dedifferentiation

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 52-OR
Author(s):  
TRACY C.S. MAK ◽  
MATHIEU LATREILLE
Keyword(s):  
Mouse Model ◽  
Beta Cell ◽  
Pancreatic Beta Cell ◽  
Cell Dedifferentiation

1875-P: The Impact of Carbohydrate/Fat Intake Balance on Beta-Cell Dedifferentiation and Fatty Liver in Obese Mouse Model

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1875-P ◽  
Author(s):  
EMI ISHIDA ◽  
XIAO LEI ◽  
EIJIRO YAMADA ◽  
SHUICHI OKADA ◽  
MASANOBU YAMADA
Keyword(s):  
Mouse Model ◽  
Beta Cell ◽  
Fatty Liver ◽  
Obese Mouse ◽  
Fat Intake ◽  
Cell Dedifferentiation ◽  
The Impact

scholarly journals APPL1 prevents pancreatic beta cell death and inflammation by dampening NFκB activation in a mouse model of type 1 diabetes

Diabetologia ◽  
2016 ◽  
Vol 60 (3) ◽  
pp. 464-474 ◽  
Author(s):  
Xue Jiang ◽  
Yawen Zhou ◽  
Kelvin K. L. Wu ◽  
Zhanrui Chen ◽  
Aimin Xu ◽  
...  
Keyword(s):  
Cell Death ◽  
Type 1 Diabetes ◽  
Mouse Model ◽  
Beta Cell ◽  
Pancreatic Beta Cell ◽  
Beta Cell Death

323-LB: Activation of the GLP-1 Receptor Signaling Prevents Beta-Cell Dedifferentiation in a Mouse Model of Wolfram Syndrome through Modulating TXNIP Expression

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 323-LB
Author(s):  
KATSUYA TANABE ◽  
KIKUKO AMO-SHIINOKI ◽  
MASAYUKI HATANAKA ◽  
YUKIO TANIZAWA
Keyword(s):  
Mouse Model ◽  
Beta Cell ◽  
Wolfram Syndrome ◽  
Receptor Signaling ◽  
Cell Dedifferentiation

scholarly journals Modeling human pancreatic beta cell dedifferentiation

2018 ◽  
Vol 10 ◽  
pp. 74-86 ◽  
Author(s):  
Marc Diedisheim ◽  
Masaya Oshima ◽  
Olivier Albagli ◽  
Charlotte Wennberg Huldt ◽  
Ingela Ahlstedt ◽  
...  
Keyword(s):  
Beta Cell ◽  
Pancreatic Beta Cell ◽  
Cell Dedifferentiation

scholarly journals Defective exocytosis and processing of insulin in a cystic fibrosis mouse model

2019 ◽  
Vol 241 (1) ◽  
pp. 45-57 ◽  
Author(s):  
A Edlund ◽  
M Barghouth ◽  
M Hühn ◽  
M Abels ◽  
J S E Esguerra ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Mouse Model ◽  
Beta Cell ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Hormone Secretion ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Cell Number

Cystic fibrosis-related diabetes (CFRD) is a common complication for patients with cystic fibrosis (CF), a disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR). The cause of CFRD is unclear, but a commonly observed reduction in first-phase insulin secretion suggests defects at the beta cell level. Here we aimed to examine alpha and beta cell function in the Cftr tm1 EUR/F508del mouse model (C57BL/6J), which carries the most common human mutation in CFTR, the F508del mutation. CFTR expression, beta cell mass, insulin granule distribution, hormone secretion and single cell capacitance changes were evaluated using islets (or beta cells) from F508del mice and age-matched wild type (WT) mice aged 7–10 weeks. Granular pH was measured with DND-189 fluorescence. Serum glucose, insulin and glucagon levels were measured in vivo, and glucose tolerance was assessed using IPGTT. We show increased secretion of proinsulin and concomitant reduced secretion of C-peptide in islets from F508del mice compared to WT mice. Exocytosis and number of docked granules was reduced. We confirmed reduced granular pH by CFTR stimulation. We detected decreased pancreatic beta cell area, but unchanged beta cell number. Moreover, the F508del mutation caused failure to suppress glucagon secretion leading to hyperglucagonemia. In conclusion, F508del mice have beta cell defects resulting in (1) reduced number of docked insulin granules and reduced exocytosis and (2) potential defective proinsulin cleavage and secretion of immature insulin. These observations provide insight into the functional role of CFTR in pancreatic islets and contribute to increased understanding of the pathogenesis of CFRD.

Metabolic Insufficiency Caused By Cellular Stresses Is Implicated in Beta-Cell Dedifferentiation in the Mouse Model of Wolfram Syndrome

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2105-P
Author(s):  
KIKUKO AMO-SHIINOKI ◽  
KATSUYA TANABE ◽  
MASAYUKI HATANAKA ◽  
YUKIO TANIZAWA
Keyword(s):  
Mouse Model ◽  
Beta Cell ◽  
Wolfram Syndrome ◽  
Cell Dedifferentiation ◽  
Cellular Stresses

Contribution of insulin signaling to the regulation of pancreatic beta-cell mass during the catch-up growth period in a low birth weight mouse model

2013 ◽  
Vol 5 (1) ◽  
pp. 43-52 ◽  
Author(s):  
Yuri Yoshida ◽  
Megumi Fuchita ◽  
Maki Kimura-Koyanagi ◽  
Ayumi Kanno ◽  
Tomokazu Matsuda ◽  
...  
Keyword(s):  
Birth Weight ◽  
Mouse Model ◽  
Beta Cell ◽  
Insulin Signaling ◽  
Pancreatic Beta Cell ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Growth Period ◽  
Catch Up ◽  
Pancreatic Beta Cell Mass

scholarly journals Enhanced Characterization of Beta Cell Mass in a Tg(Pdx1-GFP) Mouse Model of Beta Cell Destruction

2021 ◽  
Author(s):  
Fatemeh Karami ◽  
Behrouz Asgari Abibeiglou ◽  
Saghar Pahlavanneshan ◽  
Ali Farrokhi ◽  
Amin Tamadon ◽  
...  
Keyword(s):  
Mouse Model ◽  
Beta Cell ◽  
Transgenic Mouse ◽  
Beta Cells ◽  
Mass Measurement ◽  
Pancreatic Beta Cell ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Beta Cell Destruction ◽  
Cell Destruction

Abstract IntroductionMeasurement of pancreatic beta cell mass in animal models is a common assay in diabetes researches. Novel whole-organ clearance methods in conjunction with transgenic mouse models hold tremendous promise to improve methods for beta cell mass measurement. Here, we propose a refined method to estimate the beta cell mass using a new transgenic Tg(Pdx1-GFP) mouse model and a recently developed free-of-acrylamide clearing tissue (FACT) protocol. MethodsFirst, we generated and evaluated a Tg(Pdx1-GFP) transgenic mouse model. By using the FACT protocol in this model, we could quantify the beta cell mass and alloxan-induced beta cell destruction in whole pancreas specimens.ResultsTg(Pdx1-GFP) transgenic mice expressed green fluorescent protein (GFP) only in the beta cells of the pancreas and limited to the beta cells. This GFP expression enabled us to accurately measure beta cell loss in a beta cell destruction model. The results suggest that our proposed method can be used as a simple, rapid assay for beta cell mass measurement in studies of islet biology and diabetes.ConclusionThe Tg(Pdx1-GFP) transgenic mouse in conjunction with the FACT protocol can enhance large-scale screening studies in the field of diabetes.

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