Regulation of Islet  -Cell Proliferation by Prolactin in Rat Islets

Diabetes ◽  
1994 ◽  
Vol 43 (2) ◽  
pp. 263-273 ◽  
Author(s):  
T. C. Brelje ◽  
J. A. Parsons ◽  
R. L. Sorenson
Keyword(s):  
Cell Proliferation ◽  
Islet Cell ◽  
Rat Islets

scholarly journals Identification of a small molecule that stimulates human β-cell proliferation and insulin secretion, and protects against cytotoxic stress in rat insulinoma cells

2019 ◽  
Author(s):  
Hans E. Hohmeier ◽  
Lu Zhang ◽  
Brandon Taylor ◽  
Samuel Stephens ◽  
Peter McNamara ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Insulin Secretion ◽  
Small Molecule ◽  
Islet Cell ◽  
Human Islet ◽  
Luciferase Reporter ◽  
Β Cell ◽  
Cytotoxic Stress ◽  
Insulinoma Cells ◽  
Rat Insulinoma

AbstractA key event in the development of both major forms of diabetes is the loss of functional pancreatic islet β-cell mass. Strategies aimed at enhancing β-cell regeneration have long been pursued, but methods for reliably inducing human β-cell proliferation with full retention of key functions such as glucose-stimulated insulin secretion (GSIS) are still very limited. We have previously reported that overexpression of the homeobox transcription factor Nkx6.1 stimulates β-cell proliferation, while also enhancing GSIS and providing protection against β-cell cytotoxicity through induction of the VGF prohormone. We developed an Nkx6.1 pathway screen by stably transfecting 832/13 rat insulinoma cells with a VGF promoter-luciferase reporter construct, using the resultant cell line to screen a 630,000 compound chemical library. We isolated three compounds with consistent effects to stimulate human islet cell proliferation. Further studies of the most potent of these compounds, GNF-9228, revealed that it selectively activates human β-cell relative to α-cell proliferation and has no effect on δ-cell replication. In addition, pre-treatment, but not short term exposure of human islets to GNF-9228 enhances GSIS. GNF-9228 also protects 832/13 insulinoma cells against ER stress- and inflammatory cytokine-induced cytotoxicity. In contrast to recently emergent Dyrk1a inhibitors that stimulate human islet cell proliferation, GNF-9228 does not activate NFAT translocation. These studies have led to identification of a small molecule with pleiotropic positive effects on islet biology, including stimulation of human β-cell proliferation and insulin secretion, and protection against multiple agents of cytotoxic stress.

SSTR5 regulates pancreas gene expression and islet cell proliferation: A microarray analysis

2006 ◽  
Vol 130 (2) ◽  
pp. 302-303
Author(s):  
X. Wang ◽  
Z. Li ◽  
J. Jeong ◽  
S. Liu ◽  
J. Magnusson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Microarray Analysis ◽  
Islet Cell

Smad signaling plays a key role in regulating islet cell proliferation and development

2011 ◽  
Vol 213 (3) ◽  
pp. S86
Author(s):  
Yousef El-Gohary ◽  
Sidhartha Tulachan ◽  
Ping Guo ◽  
Carey Welsh ◽  
Krishna Prasadan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Islet Cell ◽  
Smad Signaling

scholarly journals Sorafenib Inhibits Tumor Growth and Improves Survival in a Transgenic Mouse Model of Pancreatic Islet Cell Tumors

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Volker Fendrich ◽  
Katja Maschuw ◽  
Johannes Rehm ◽  
Malte Buchholz ◽  
Julia P. Holler ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Treatment Group ◽  
Tumor Progression ◽  
Early Treatment ◽  
Islet Cell ◽  
Control Group ◽  
Islet Cell Tumors ◽  
Pancreatic Islet Cell ◽  
Early Treatment Group ◽  
Late Treatment

Background. The purpose of the study was to evaluate Sorafenib (BAY 43-9006) derived receptor tyrosine kinase inhibition on tumor progression in murine islet cell tumors. Sorafenib is considered to be a potent inhibitor of tumor angiogenesis and neovascularization in various solid tumors. Rip1Tag2 mice were treated in two different groups according to the model of tumor progression: the early treatment group received vehicle or Sorafenib from 10 to 14 weeks of age and the late treatment group from week 12 until death. Tumor surface, tumor cell proliferation, and apoptosis were measured in both treatment groups to assess the in vivo effects of Sorafenib. Survival was recorded for the late treatment group. In the early treatment group Sorafenib led to a dramatic decrease in tumor volume compared to the control group. Apoptosis was significantly augmented and cell proliferation was inhibited. As a single therapy Sorafenib significantly improved survival in the late treatment group.Conclusion. Sorafenib may provide a new paradigm for the therapy of islet cell tumors.

scholarly journals 17β-Estradiol Promotes Islet Cell Proliferation in a Partial Pancreatectomy Mouse Model

2017 ◽  
Vol 1 (7) ◽  
pp. 965-979 ◽  
Author(s):  
Tingting Wu ◽  
Jinyong Xu ◽  
Shengchun Xu ◽  
Lianzhong Wu ◽  
Youyu Zhu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mouse Model ◽  
Islet Cell ◽  
Partial Pancreatectomy ◽  
17Β Estradiol

scholarly journals Distinct antibody specificities to a 64-kD islet cell antigen in type 1 diabetes as revealed by trypsin treatment.

1990 ◽  
Vol 172 (3) ◽  
pp. 789-794 ◽  
Author(s):  
M R Christie ◽  
G Vohra ◽  
P Champagne ◽  
D Daneman ◽  
T L Delovitch
Keyword(s):  
Type 1 Diabetes ◽  
Islet Cell ◽  
Positive Association ◽  
Diagnostic Value ◽  
Diabetic Patients ◽  
Trypsin Treatment ◽  
Rat Islets ◽  
Antibody Specificities ◽  
64K Antibodies

Type 1 diabetes is associated with antibodies that immunoprecipitate a 64-kD islet cell membrane protein from detergent extracts of pancreatic islets. In this study we have determined whether mild trypsin treatment of islet membranes can release fragments of the antigen that bind antibodies in the serum of Type 1 diabetic patients. Partial tryptic proteolysis of [35S]methionine-labeled 64-kD antigen immunoprecipitated from detergent extracts of rat islets resulted in the formation of 50-, 40-, and 37-kD fragments. Similar sized fragments were recovered when sera from diabetic patients were employed to immunoprecipitate polypeptides solubilized by mild trypsin treatment of a particulate fraction of radiolabeled rat islets. Of 27 diabetic patients, 22 possessed antibodies to the 50-kD polypeptide and 21 to the 40- and 37-kD polypeptides. A positive association was found between 64k antibodies and antibodies to the 50-kD fragment but not between 64k antibodies and antibodies to the 40- or 37-kD fragments. Some 64k antibody negative patients possessed antibodies that efficiently immunoprecipitated the latter fragments. Serum from 25 of 27 (93%) diabetic patients immunoprecipitated at least one of the three tryptic polypeptides. One of 20 nondiabetic controls immunoprecipitated a 50-kD polypeptide and all controls were negative for antibodies to 40- and 37-kD fragments. Thus, Type 1 diabetes is associated with the presence of at least two antibody reactivities to distinct determinants of the 64-kD antigen, and some patients may possess antibodies to a cryptic epitope on the detergent-solubilized molecule. These data suggest that the detection of antibodies (present in 93% of patients) to epitopes on tryptic polypeptides of the 64-kD antigen may be of even greater diagnostic value for the onset of Type 1 diabetes than analyses of antibodies reactive with the intact 64-kD antigen.

scholarly journals A Smad Signaling Network Regulates Islet Cell Proliferation

Diabetes ◽  
2013 ◽  
Vol 63 (1) ◽  
pp. 224-236 ◽  
Author(s):  
Y. El-Gohary ◽  
S. Tulachan ◽  
J. Wiersch ◽  
P. Guo ◽  
C. Welsh ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Islet Cell ◽  
Signaling Network ◽  
Smad Signaling

scholarly journals Superior beta cell proliferation, function and gene expression in a subpopulation of rat islets identified by high blood perfusion

Diabetologia ◽  
2012 ◽  
Vol 55 (5) ◽  
pp. 1390-1399 ◽  
Author(s):  
J. Lau ◽  
J. Svensson ◽  
L. Grapensparr ◽  
Å. Johansson ◽  
P.-O. Carlsson
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Beta Cell ◽  
Blood Perfusion ◽  
Beta Cell Proliferation ◽  
Rat Islets
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