Cis‐regulation of antisense noncoding RNA at the JAZF1 locus in type 2 diabetes

Author(s):  
Qiuju Ding ◽  
Weiwei Zhao ◽  
Jirong Long ◽  
Habiba Alsafar ◽  
Qing Zhou ◽  
...  
Author(s):  
Hanlu Fan ◽  
Haiwen Li ◽  
Huijiao Liu ◽  
Peng Li ◽  
Xiaomeng Jia ◽  
...  

Abstract Background Type 2 diabetes mellitus (T2DM) is the most common type of metabolic disorder involving multiple organ systems. Grape has been reported to improve the symptoms of T2DM, the precise mechanism of its action is unclear. Our study was aimed to determine the effect and mechanism of grape pomace extract in T2DM mice induced by high fat diet (HFD). Materials and methods Ultra-performance liquid chromatography and quadrupole time-of-flight mass spectrometry were used to identify the main active compounds in grape pomace extract to improve T2DM. C57BLK/6J mice induced by HFD supplemented with or without quercetin were used to show the effects of quercetin improving T2DM. By online database research, bioinformatics analysis and molecular biology experiments, Estrogen receptor alpha (ERα)-lncSHGL (lncRNA suppressor of hepatic gluconeogenesis and lipogenesis) pathway was identify as the target for quercetin. Results Quercetin was identified as one of the most active compounds in grape pomace extract to improve T2DM. Quercetin could inhibit HFD-induced T2DM in mice by activing ERα. LncSHGL was identified as the downstream of ERα and inhibited HFD-induced T2DM. Conclusions Quercetin could be beneficial for T2DM by promoting lncSHGL transcription and activating the lncSHGL pathway, and may be used as a drug component to treat T2DM.


Gene ◽  
2018 ◽  
Vol 675 ◽  
pp. 265-271 ◽  
Author(s):  
Hamid Ghaedi ◽  
Ali Zare ◽  
Mir Davood Omrani ◽  
Amir Hossein Doustimotlagh ◽  
Reza Meshkani ◽  
...  

Author(s):  
Mahroo Mohamadi ◽  
Hamid Ghaedi ◽  
Faranak Kazerouni ◽  
Maryam Erfanian Omidvar ◽  
Saeid Kalbasi ◽  
...  

2021 ◽  
Vol 22 (2) ◽  
pp. 496
Author(s):  
Maria Nicol Arroyo ◽  
Jonathan Alex Green ◽  
Miriam Cnop ◽  
Mariana Igoillo-Esteve

The global rise in type 2 diabetes results from a combination of genetic predisposition with environmental assaults that negatively affect insulin action in peripheral tissues and impair pancreatic β-cell function and survival. Nongenetic heritability of metabolic traits may be an important contributor to the diabetes epidemic. Transfer RNAs (tRNAs) are noncoding RNA molecules that play a crucial role in protein synthesis. tRNAs also have noncanonical functions through which they control a variety of biological processes. Genetic and environmental effects on tRNAs have emerged as novel contributors to the pathogenesis of diabetes. Indeed, altered tRNA aminoacylation, modification, and fragmentation are associated with β-cell failure, obesity, and insulin resistance. Moreover, diet-induced tRNA fragments have been linked with intergenerational inheritance of metabolic traits. Here, we provide a comprehensive review of how perturbations in tRNA biology play a role in the pathogenesis of monogenic and type 2 diabetes.


Author(s):  
Lei Wan ◽  
Xinying Song ◽  
Baoqing Zhu

IntroductionType 2 diabetes mellitus (T2DM) is a major kind of diabetes mellitus. This study aimed to analyze the regulatory effect of long noncoding RNA NBR2 on pancreatic  cell function and the related mechanisms, and to analyze the clinical significance of abnormal NBR2 expression in patients with T2DM.Material and methodsThe expression levels of NBR2 and microRNA-19a-3p (miR-19a-3p) were measured using quantitative Real-Time PCR. The glucose-stimulated insulin secretion was measured using ELISA kit, and cell proliferation was examined using Cell Counting Kit-8 (CCK-8) assay. A dual-luciferase reporter assay was used to confirm the relationship between NBR2 and miR-19a-3p. The diagnostic values of NBR2, miR-19a-3p and NBR2 combined with miR-19a-3p were assessed by receiver operating characteristic (ROC) curves.ResultsThe insulin secretion and proliferation of INS-1 cells were inhibited by NBR2 overexpression, and were promoted by NBR2 knockdown. MiR-19a-3p, which was inhibited by NBR2 overexpression, directly mediated the regulatory effects of NBR2 on INS-1 cell function. Increased serum NBR2 level and decreased serum miR-19a-3p level were found in T2DM patients, and a negative correlation was found between NBR2 and miR-19a-3p. The fasting plasma glucose of T2DM patients was positively correlated with serum NBR2 and negatively correlated with serum miR-19a-3p. Both serum NBR2 and miR-19a-3p had certain diagnostic accuracy, whereas, the combined detection of the serum NBR2 and miR-19a-3p showed more considerable diagnostic accuracy.ConclusionsOur findings indicated that NBR2/miR-19a-3p axis regulates pancreatic β cell function, while may be novel biomarkers for the diagnosis of T2DM.


BBA Clinical ◽  
2015 ◽  
Vol 4 ◽  
pp. 102-107 ◽  
Author(s):  
Gay Carter ◽  
Branko Miladinovic ◽  
Achintya A. Patel ◽  
Lauren Deland ◽  
Stephen Mastorides ◽  
...  

2018 ◽  
Vol 120 (6) ◽  
pp. 9315-9323 ◽  
Author(s):  
Maryam Erfanian Omidvar ◽  
Hamid Ghaedi ◽  
Faranak Kazerouni ◽  
Saeid kalbasi ◽  
Mehrnoosh Shanaki ◽  
...  

2017 ◽  
Vol 92 ◽  
pp. 445-450 ◽  
Author(s):  
Zhuo Zhao ◽  
Bin Liu ◽  
Bo Li ◽  
Chunli Song ◽  
Hongying Diao ◽  
...  

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