scholarly journals Islet amyloid polypeptide promotes beta-cell proliferation in neonatal rat pancreatic islets

Diabetologia ◽  
2001 ◽  
Vol 44 (8) ◽  
pp. 1015-1018 ◽  
Author(s):  
E. Karlsson ◽  
S. Sandler
Diabetologia ◽  
2009 ◽  
Vol 53 (2) ◽  
pp. 396-396
Author(s):  
J. Olerud ◽  
N. Kanaykina ◽  
S. Vasylovska ◽  
D. King ◽  
M. Sandberg ◽  
...  

2022 ◽  
Author(s):  
Hannah J MacMillan ◽  
Yahui Kong ◽  
Ezequiel Calvo-Roitberg ◽  
Laura C Alonso ◽  
Athma A Pai

The antisense non-coding RNA in the INK locus (ANRIL) is a hotspot for genetic variants associated with cardiometabolic disease. We recently found increased ANRIL abundance in human pancreatic islets from donors with certain Type II Diabetes (T2D) risk-SNPs, including a T2D risk-SNP located within ANRIL exon 2 associated with beta cell proliferation. Recent studies have found that expression of circular species of ANRIL is linked to the regulation of cardiovascular phenotypes. Less is known about how the abundance of circular ANRIL may influence T2D phenotypes. Herein, we sequence circular RNA in pancreatic islets to characterize circular isoforms of ANRIL. We identify highly expressed circular ANRIL isoforms whose expression is correlated across dozens of individuals and characterize ANRIL splice sites that are commonly involved in back-splicing. We find that samples with the T2D risk allele in ANRIL exon 2 had higher ratios of circular to linear ANRIL compared to protective-allele carriers, and that higher circular:linear ANRIL was associated with decreased beta cell proliferation. Our study points to a combined involvement of both linear and circular ANRIL species in T2D phenotypes and opens the door for future studies of the molecular mechanisms by which ANRIL impacts cellular function in pancreatic islets.


Diabetologia ◽  
2009 ◽  
Vol 52 (12) ◽  
pp. 2594-2601 ◽  
Author(s):  
J. Olerud ◽  
N. Kanaykina ◽  
S. Vasilovska ◽  
D. King ◽  
M. Sandberg ◽  
...  

1999 ◽  
Vol 276 (1) ◽  
pp. E19-E24 ◽  
Author(s):  
Feng Wang ◽  
Thomas E. Adrian ◽  
Gunilla T. Westermark ◽  
Xianzhong Ding ◽  
Thomas Gasslander ◽  
...  

Islet amyloid polypeptide (IAPP, or amylin) is produced in pancreatic β-cells. The intraislet significance of IAPP is still uncertain. In the present study, paracrine effects of endogenous IAPP and somatostatin were investigated in isolated rat pancreatic islets. The intraislet IAPP activity was inhibited with an IAPP antiserum or a specific antagonist [IAPP-(8—37)]. Somatostatin activity was inhibited by immunoneutralization. Basal insulin and glucagon secretion were not affected by the somatostatin and/or IAPP blockade. Arginine-stimulated insulin and glucagon secretion were dose dependently increased by IAPP antiserum, IAPP-(8—37), and somatostatin antiserum, respectively. Arginine-stimulated somatostatin secretion was dose dependently potentiated by IAPP antiserum. Insulin secretion induced by 16.7 mM glucose was enhanced by IAPP antiserum and IAPP-(8—37), respectively. A combination of somatostatin antiserum with IAPP antiserum or IAPP-(8—37) further enhanced the arginine-stimulated insulin and glucagon secretion compared with effects when the blocking reagents were used individually. These results indicate that endogenously produced IAPP tonally inhibits stimulated insulin, glucagon, and somatostatin secretion. Furthermore, the paracrine effects of IAPP and somatostatin are additive.


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