scholarly journals Insulitis and β-Cell Mass in the Natural History of Type 1 Diabetes

Diabetes ◽  
2015 ◽  
Vol 65 (3) ◽  
pp. 719-731 ◽  
Author(s):  
Martha Campbell-Thompson ◽  
Ann Fu ◽  
John S. Kaddis ◽  
Clive Wasserfall ◽  
Desmond A. Schatz ◽  
...  
2019 ◽  
Vol 15 (5) ◽  
pp. 256-257 ◽  
Author(s):  
Paolo Pozzilli ◽  
Alberto Signore

Diabetes ◽  
2015 ◽  
Vol 64 (6) ◽  
pp. 2148-2160 ◽  
Author(s):  
Helena Chmelova ◽  
Christian M. Cohrs ◽  
Julie A. Chouinard ◽  
Cathleen Petzold ◽  
Matthias Kuhn ◽  
...  

2016 ◽  
Vol 64 (1) ◽  
pp. 14-20 ◽  
Author(s):  
Ercument Dirice ◽  
Rohit N Kulkarni

Type 1 diabetes is characterized by early β-cell loss leading to insulin dependence in virtually all patients with the disease in order to maintain glucose homeostasis. Most studies over the past few decades have focused on limiting the autoimmune attack on the β cells. However, emerging data from patients with long-standing diabetes who continue to harbor functional insulin-producing cells in their diseased pancreas have prompted scientists to examine whether proliferation of existing β cells can be enhanced to promote better glycemic control. In support of this concept, several studies indicate that mononuclear cells that infiltrate the islets have the capacity to trigger proliferation of islet cells including β cells. These observations indicate the exciting possibility of identifying those mononuclear cell types and their soluble factors and harnessing their ability to promote β-cell growth concomitant with autoimmune therapy to prevent the onset and/or halt the progression of the disease.


1999 ◽  
Vol 44 ◽  
pp. S26
Author(s):  
S. Salardi ◽  
S. Zucchini ◽  
L. Ragni ◽  
B. Mainetti ◽  
E. Cacciari

2009 ◽  
Vol 25 (4) ◽  
pp. 325-328 ◽  
Author(s):  
Jerry P. Palmer

Diabetes ◽  
2012 ◽  
Vol 62 (1) ◽  
pp. 44-48 ◽  
Author(s):  
Patrick F. Antkowiak ◽  
Brian K. Stevens ◽  
Craig S. Nunemaker ◽  
Marcia McDuffie ◽  
Frederick H. Epstein

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