scholarly journals Circular RNAs as Novel Regulators of β-Cell Functions under Physiological and Pathological Conditions

2021 ◽  
Vol 22 (4) ◽  
pp. 1503 ◽  
Author(s):  
Flora Brozzi ◽  
Romano Regazzi
Keyword(s):  
Islet Cells ◽  
Circular Rnas ◽  
Diabetic Patients ◽  
Β Cell ◽  
Type 2 Diabetic Patients ◽  
Altered Expression ◽  
Cell Functions ◽  
Pathological Conditions ◽  
Mrna Maturation

Circular RNAs (circRNAs) constitute a large class of non-coding RNAs characterized by a covalently closed circular structure. They originate during mRNA maturation through a modification of the splicing process and, according to the included sequences, are classified as Exonic, Intronic, or Exonic-Intronic. CircRNAs can act by sequestering microRNAs, by regulating the activity of specific proteins, and/or by being translated in functional peptides. There is emerging evidence indicating that dysregulation of circRNA expression is associated with pathological conditions, including cancer, neurological disorders, cardiovascular diseases, and diabetes. The aim of this review is to provide a comprehensive and updated view of the most abundant circRNAs expressed in pancreatic islet cells, some of which originating from key genes controlling the differentiation and the activity of insulin-secreting cells or from diabetes susceptibility genes. We will particularly focus on the role of a group of circRNAs that contribute to the regulation of β-cell functions and that display altered expression in the islets of rodent diabetes models and of type 2 diabetic patients. We will also provide an outlook of the unanswered questions regarding circRNA biology and discuss the potential role of circRNAs as biomarkers for β-cell demise and diabetes development.

Role of Oxidative Stress and Mitochondrial Dysfunction in Skeletal Muscle in Type 2 Diabetic Patients

2016 ◽  
Vol 22 (18) ◽  
pp. 2650-2656 ◽  
Author(s):  
Noelia Diaz-Morales ◽  
Susana Rovira-Llopis ◽  
Irene Escribano-Lopez ◽  
Celia Bañuls ◽  
Sandra Lopez-Domenech ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Mitochondrial Dysfunction ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Type 2 Diabetic

Evaluation of apolipoprotein E secretion by macrophages in type 2 diabetic patients: role of HDL and apolipoprotein A-I

2005 ◽  
Vol 69 (2) ◽  
pp. 124-128 ◽  
Author(s):  
Kazumi Yamato ◽  
Naoki Tamasawa ◽  
Hiroshi Murakami ◽  
Jun Matsui ◽  
Jutaro Tanabe ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Apolipoprotein A ◽  
Type 2 Diabetic

scholarly journals Non-Coding RNA in Pancreas and β-Cell Development

2018 ◽  
Vol 4 (4) ◽  
pp. 41 ◽  
Author(s):  
Wilson K. M. Wong ◽  
Anja E. Sørensen ◽  
Mugdha V. Joglekar ◽  
Anand A. Hardikar ◽  
Louise T. Dalgaard
Keyword(s):  
Cell Function ◽  
Islet Cells ◽  
Current Knowledge ◽  
Cell Development ◽  
Pancreas Development ◽  
Β Cell ◽  
Neighboring Gene ◽  
Non Coding Rnas ◽  
And Function

In this review, we provide an overview of the current knowledge on the role of different classes of non-coding RNAs for islet and β-cell development, maturation and function. MicroRNAs (miRNAs), a prominent class of small RNAs, have been investigated for more than two decades and patterns of the roles of different miRNAs in pancreatic fetal development, islet and β-cell maturation and function are now emerging. Specific miRNAs are dynamically regulated throughout the period of pancreas development, during islet and β-cell differentiation as well as in the perinatal period, where a burst of β-cell replication takes place. The role of long non-coding RNAs (lncRNA) in islet and β-cells is less investigated than for miRNAs, but knowledge is increasing rapidly. The advent of ultra-deep RNA sequencing has enabled the identification of highly islet- or β-cell-selective lncRNA transcripts expressed at low levels. Their roles in islet cells are currently only characterized for a few of these lncRNAs, and these are often associated with β-cell super-enhancers and regulate neighboring gene activity. Moreover, ncRNAs present in imprinted regions are involved in pancreas development and β-cell function. Altogether, these observations support significant and important actions of ncRNAs in β-cell development and function.

Hyperhomocysteinemia and elevated ox-LDL in Tunisian type 2 diabetic patients: Role of genetic and dietary factors

2007 ◽  
Vol 40 (13-14) ◽  
pp. 1007-1014 ◽  
Author(s):  
N. Koubaa ◽  
A. Nakbi ◽  
M. Smaoui ◽  
N. Abid ◽  
R. Chaaba ◽  
...  
Keyword(s):  
Dietary Factors ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Type 2 Diabetic

Investigating ADAMTS7 and ADAMTS12 levels in prediabetic and Type 2 diabetic patients

2021 ◽  
Author(s):  
Mercan Taştemur ◽  
Selvihan Beysel ◽  
Sema Hepşen ◽  
Sanem Öztekin ◽  
Erman Çakal ◽  
...  
Keyword(s):  
Inflammatory Markers ◽  
Diabetic Patients ◽  
Control Groups ◽  
Type 2 Diabetic Patients ◽  
Human Enzyme ◽  
Significant Difference ◽  
And Control ◽  
Type 2 Diabetic

Background: This study aims to investigate the role of ADAMTS7 and ADAMTS12 on atherosclerosis and inflammation in prediabetic and diabetic patients. Patients & methods: Serum ADAMTS7 and ADAMTS12 levels were compared with the atherosclerotic and inflammatory markers in diabetic (n = 65, female 30.9%, mean age = 53 years), prediabetic (n = 55, female 36.6%, mean age = 49 years) and control groups (n = 55, females 32.5%, mean age = 49 years). Serum ADAMTS levels were determined by a human enzyme-liked immunoassay. Results: In terms of ADAMTS7, there was no significant difference between diabetic, prediabetic and control groups (50.93, 44.34, 59.07, respectively; p > 0.05). ADAMTS12 is lower in diabetics (p < 0.05), whereas it is similar in prediabetics and controls (14.53, 20.76, 25.05, respectively; p > 0.05). ADAMTS7 and ADAMTS12 levels did not differ in diabetic nephropathy, retinopathy and neuropathy (p > 0.05). Conclusion: While ADAMTS12 was significantly lower in diabetics and prediabetics, ADAMTS7 and ADAMTS12 were not related to diabetic complications (nephropathy, retinopathy and neuropathy).

scholarly journals Resveratrol improves insulin sensitivity, reduces oxidative stress and activates the Akt pathway in type 2 diabetic patients

2011 ◽  
Vol 106 (3) ◽  
pp. 383-389 ◽  
Author(s):  
Pál Brasnyó ◽  
Gergő A. Molnár ◽  
Márton Mohás ◽  
Lajos Markó ◽  
Boglárka Laczy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Cell Function ◽  
Diabetic Patients ◽  
Β Cell ◽  
Type 2 Diabetic Patients ◽  
Β Cell Function ◽  
Type 2 Diabetic

Although resveratrol has widely been studied for its potential health benefits, little is known about its metabolic effects in humans. Our aims were to determine whether the polyphenol resveratrol improves insulin sensitivity in type 2 diabetic patients and to gain some insight into the mechanism of its action. After an initial general examination (including blood chemistry), nineteen patients enrolled in the 4-week-long double-blind study were randomly assigned into two groups: a resveratrol group receiving oral 2 × 5 mg resveratrol and a control group receiving placebo. Before and after the second and fourth weeks of the trial, insulin resistance/sensitivity, creatinine-normalised ortho-tyrosine level in urine samples (as a measure of oxidative stress), incretin levels and phosphorylated protein kinase B (pAkt):protein kinase B (Akt) ratio in platelets were assessed and statistically analysed. After the fourth week, resveratrol significantly decreased insulin resistance (homeostasis model of assessment for insulin resistance) and urinary ortho-tyrosine excretion, while it increased the pAkt:Akt ratio in platelets. On the other hand, it had no effect on parameters that relate to β-cell function (i.e. homeostasis model of assessment of β-cell function). The present study shows for the first time that resveratrol improves insulin sensitivity in humans, which might be due to a resveratrol-induced decrease in oxidative stress that leads to a more efficient insulin signalling via the Akt pathway.

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