Beta-cell insensitivity to glucose in the GK rat, a spontaneous nonobese model for type II diabetes

Diabetes ◽  
1991 ◽  
Vol 40 (4) ◽  
pp. 486-491 ◽  
Author(s):  
B. Portha ◽  
P. Serradas ◽  
D. Bailbe ◽  
K. Suzuki ◽  
Y. Goto ◽  
...  
Keyword(s):  
Type Ii ◽  
2017 ◽  
Vol 28 (4) ◽  
pp. 282-286
Author(s):  
Yi Yuan Zhou ◽  
Soufiane El Hallani ◽  
Fady Balaa ◽  
Waleed Mohammad ◽  
Douglas A. Gray ◽  
...  

Diabetologia ◽  
2001 ◽  
Vol 44 (10) ◽  
pp. 1330-1334 ◽  
Author(s):  
T. Hansen ◽  
L. Ambye ◽  
N. Grarup ◽  
L. Hansen ◽  
S. M. Echwald ◽  
...  

1983 ◽  
Vol 15 (12) ◽  
pp. 575-580
Author(s):  
I. Toledo e Souza ◽  
B. Wajchenberg ◽  
F. Cesar ◽  
J. Almeida Neto

2000 ◽  
Vol 24 (3) ◽  
pp. 303-311 ◽  
Author(s):  
CJ Rhodes

Certain nutrients, pharmacological agents and growth factors can stimulate pancreatic beta-cell proliferation; however, mitogenic signal transduction pathways in beta-cells have not been particularly well characterized. As a model system we have focussed on characterizing the signal transduction pathways immediately downstream of the IGF-I and GH receptors in beta-cells. The original idea was to gain an idea of important elements in mitogenic signaling pathways which might then be exploited to generate a marked increase in beta-cell proliferation. Such an approach could eventually reveal a means to increase the number of human pancreatic endocrine cells in vitro, in order to obtain an abundant source of beta-cells for routine transplantation therapy of type-I diabetes. However, in the course of our studies, we have also unveiled an unexpected insight into the pathogenesis of obesity-linked type-II diabetes. It has been observed that free fatty acids inhibit glucose- and glucose-dependent IGF-I/GH-induced beta-cell proliferation. We hypothesize that a gradual accumulation of intracellular fat in beta-cells during obesity can eventually lead to an inhibition of beta-cell mass expansion and hence failure to compensate for peripheral insulin resistance, so that type-II diabetes ensues.


Diabetes ◽  
1991 ◽  
Vol 40 (4) ◽  
pp. 486-491 ◽  
Author(s):  
B. Portha ◽  
P. Serradas ◽  
D. Bailbe ◽  
K.-I. Suzuki ◽  
Y. Goto ◽  
...  
Keyword(s):  
Type Ii ◽  

1994 ◽  
Vol 40 (6) ◽  
pp. 47-50 ◽  
Author(s):  
V. N. Babichev ◽  
I. P. Savelyeva ◽  
M. I. Balabolkin

Analysis of pancreatic beta-cell receptors binding the sulfanilamide drugs widely used in therapy of type II diabetes, such as glybenclamide, glypizide, and glyclazide, showed that these drugs are characterized by excellent parameters of specific binding to these receptors. The receptors were tested for two parameters: number of binding sites and dissociation constant. Glybenclamide was the most active of the drugs we tested, the other two agents being less active. Binding of these agents was reversible. The problem of identification of the examined receptors of sulfanilamides with K+-ATP-sensitive channels, similarly active conductors of the information transported by the sulfanilamide drugs in the mechanism of insulin secretion, is discussed.


Diabetes ◽  
1988 ◽  
Vol 37 (1) ◽  
pp. 99-103 ◽  
Author(s):  
L. Groop ◽  
A. Miettinen ◽  
P. H. Groop ◽  
S. Meri ◽  
S. Koskimies ◽  
...  

The Lancet ◽  
1986 ◽  
Vol 328 (8507) ◽  
pp. 628-629
Author(s):  
R.E Ferner ◽  
R.J Jarrett ◽  
R.D.G Leslie ◽  
S.P O'Rahilly ◽  
Z Nugent ◽  
...  

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