β-Cell Loss and Glucose Induced Signalling Defects in Diabetes Mellitus Caused by Mitochondrial tRNALeu(UUR) Gene Mutation

1996 ◽  
Vol 13 ◽  
pp. 98-102 ◽  
Author(s):  
Y. Oka ◽  
H. Katagiri ◽  
H. Ishihara ◽  
T. Asano ◽  
T. Kobayashi ◽  
...  
2018 ◽  
Author(s):  
TT Cui ◽  
N Hallahan ◽  
W Jonas ◽  
P Gottmann ◽  
M Jähnert ◽  
...  
Keyword(s):  

2021 ◽  
Vol 22 (2) ◽  
pp. 803
Author(s):  
Giuseppina Emanuela Grieco ◽  
Noemi Brusco ◽  
Giada Licata ◽  
Daniela Fignani ◽  
Caterina Formichi ◽  
...  

Diabetes mellitus is a group of heterogeneous metabolic disorders characterized by chronic hyperglycaemia mainly due to pancreatic β cell death and/or dysfunction, caused by several types of stress such as glucotoxicity, lipotoxicity and inflammation. Different patho-physiological mechanisms driving β cell response to these stresses are tightly regulated by microRNAs (miRNAs), a class of negative regulators of gene expression, involved in pathogenic mechanisms occurring in diabetes and in its complications. In this review, we aim to shed light on the most important miRNAs regulating the maintenance and the robustness of β cell identity, as well as on those miRNAs involved in the pathogenesis of the two main forms of diabetes mellitus, i.e., type 1 and type 2 diabetes. Additionally, we acknowledge that the understanding of miRNAs-regulated molecular mechanisms is fundamental in order to develop specific and effective strategies based on miRNAs as therapeutic targets, employing innovative molecules.


Author(s):  
Jing Yong ◽  
James D. Johnson ◽  
Peter Arvan ◽  
Jaeseok Han ◽  
Randal J. Kaufman

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 264
Author(s):  
Seon-Heui Cha ◽  
Chunying Zhang ◽  
Soo-Jin Heo ◽  
Hee-Sook Jun

Pancreatic β-cell loss is critical in diabetes pathogenesis. Up to now, no effective treatment has become available for β-cell loss. A polyphenol recently isolated from Polysiphonia japonica, 5-Bromoprotocatechualdehyde (BPCA), is considered as a potential compound for the protection of β-cells. In this study, we examined palmitate (PA)-induced lipotoxicity in Ins-1 cells to test the protective effects of BPCA on insulin-secreting β-cells. Our results demonstrated that BPCA can protect β-cells from PA-induced lipotoxicity by reducing cellular damage, preventing reactive oxygen species (ROS) overproduction, and enhancing glucose-stimulated insulin secretion (GSIS). BPCA also improved mitochondrial morphology by preserving parkin protein expression. Moreover, BPCA exhibited a protective effect against PA-induced β-cell dysfunction in vivo in a zebrafish model. Our results provide strong evidence that BPCA could be a potential therapeutic agent for the management of diabetes.


Nature ◽  
2010 ◽  
Vol 464 (7292) ◽  
pp. 1149-1154 ◽  
Author(s):  
Fabrizio Thorel ◽  
Virginie Népote ◽  
Isabelle Avril ◽  
Kenji Kohno ◽  
Renaud Desgraz ◽  
...  
Keyword(s):  
Β Cells ◽  

2018 ◽  
Vol 26 (2) ◽  
pp. e12474 ◽  
Author(s):  
Regan Roat ◽  
Md Munir Hossain ◽  
Jenica Christopherson ◽  
Colette Free ◽  
Claudiane Guay ◽  
...  

2015 ◽  
Vol 165 (1) ◽  
pp. 91-101 ◽  
Author(s):  
Justin S. Johnson ◽  
Carmella Evans-Molina
Keyword(s):  

2014 ◽  
Vol 19 (2) ◽  
pp. 162-168 ◽  
Author(s):  
Riccardo Calafiore ◽  
Pia Montanucci ◽  
Giuseppe Basta

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