83-OR: Pancreatic Exocrine to Endocrine Cell Cross Talk Mediates Endoplasmic Reticulum Stress and Beta-Cell Dysfunction in MODY8

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 83-OR
Author(s):  
SEVIM KAHRAMAN ◽  
DANIELLE DIEGISSER ◽  
BENTE B. JOHANSSON ◽  
ANDERS MOLVEN ◽  
ROHIT KULKARNI
Diabetologia ◽  
2021 ◽  
Vol 64 (11) ◽  
pp. 2534-2549
Author(s):  
Nur Shabrina Amirruddin ◽  
Wei Xuan Tan ◽  
Yaw Sing Tan ◽  
Daphne Su-Lyn Gardner ◽  
Yong Mong Bee ◽  
...  

Diabetologia ◽  
2012 ◽  
Vol 55 (5) ◽  
pp. 1366-1379 ◽  
Author(s):  
C. Tang ◽  
K. Koulajian ◽  
I. Schuiki ◽  
L. Zhang ◽  
T. Desai ◽  
...  

2011 ◽  
Vol 23 (11) ◽  
pp. 1708-1715 ◽  
Author(s):  
Margot M.L. Linssen ◽  
Daniel H. van Raalte ◽  
Erik J.M. Toonen ◽  
Wynand Alkema ◽  
Gerard C. van der Zon ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Mi-Kyung Kim ◽  
Hye-Soon Kim ◽  
In-Kyu Lee ◽  
Keun-Gyu Park

Insulin resistance and pancreatic beta cell dysfunction are major contributors to the pathogenesis of diabetes. Various conditions play a role in the pathogenesis of pancreatic beta cell dysfunction and are correlated with endoplasmic reticulum (ER) stress. Pancreatic beta cells are susceptible to ER stress. Many studies have shown that increased ER stress induces pancreatic beta cell dysfunction and diabetes mellitus using genetic models of ER stress and by various stimuli. There are many reports indicating that ER stress plays an important role in the impairment of insulin biosynthesis, suggesting that reduction of ER stress could be a therapeutic target for diabetes. In this paper, we reviewed the relationship between ER stress and diabetes and how ER stress controls insulin biosynthesis.


Diabetes ◽  
1986 ◽  
Vol 35 (2) ◽  
pp. 139-142 ◽  
Author(s):  
S. Srikanta ◽  
A. T. Ricker ◽  
D. K. McCulloch ◽  
J. S. Soeldner ◽  
G. S. Eisenbarth ◽  
...  

2017 ◽  
Vol 68 (7) ◽  
pp. 1622-1627 ◽  
Author(s):  
Diana Simona Stefan ◽  
Andrada Mihai ◽  
Daiana Bajko ◽  
Daniela Lixandru ◽  
Laura Petcu ◽  
...  

Metabolic surgery is the most efficacious method for the treatment of morbid obesity and was recently included among the antidiabetes treatments recommended in obese type 2 diabetes (T2D) patients. The aim of this study was to compare in a randomized controlled trial the effect of sleeve gastrectomy (SG) to that of intensive lifestyle intervention plus pharmacologic treatment on some markers of insulin resistance and beta cell function as well as some appetite controlling hormones in a group of male obese T2D subjects. The study groups comprised 20 subjects for SG and 21 control subjects. Fasting blood glucose, insulin, proinsulin, adiponectin, leptin, ghrelin, HOMA-IR, HOMA-%B, proinsulin-to-insulin ratio and proinsulin-to-adiponectin ratio were evaluated at baseline and after one year follow-up. Overall, patients in the SG group lost 78.98% of excess weight loss (%EWL) in comparison with 9.45% in the control group. This was accompanied by a significant improvement of insulin resistance markers, including increase of adiponectin and decrease of HOMA-IR, while no changes were recorded in the control group. Weight loss was also associated with a significant improvement of proinsulin-to-insulin and proinsulin-to-adiponectin ratio, both surrogate markers of beta cell dysfunction. These also improved in the control group, but were only marginally significant. Our findings suggest that improved insulin resistance and decreased beta cell dysfunction after sleeve gastrectomy might explain diabetes remission associated with metabolic surgery.


2017 ◽  
Vol 33 (3) ◽  
pp. 315-324 ◽  
Author(s):  
Chang Liu ◽  
Dong-Ying Yan ◽  
Xuan Tan ◽  
Zhuo Ma ◽  
Can Wang ◽  
...  

2008 ◽  
Vol 55 (2) ◽  
pp. 433-438 ◽  
Author(s):  
Yoshifumi SAISHO ◽  
Hiroshi HIROSE ◽  
Chihiro HORIMAI ◽  
Kiichi MIYASHITA ◽  
Izumi TAKEI ◽  
...  

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