Altered Expression of miR-181a-5p and miR-23a-3p Is Associated With Obesity and TNFα-Induced Insulin Resistance

Lozano-Bartolomé, Javier; Llauradó, Gemma; Portero-Otı́n, Manel; Altuna-Coy, Antonio; Rojo‐Martínez, Gemma; Vendrell, Joan; Jorba, Rosa; Rodríguez-Gallego, Esther; Chacón, Matilde R.

doi:10.1210/jc.2017-01909

Cited by 72 publications

(72 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The 3rd and 4th quintiles consisted respectively of 54 and 45 miRNAs (Supplementary Tables 2 and 3), group most of the regulators of lipid metabolism, adipogenesis and insulin resistance pathways. Among them, miR-23a, miR-26a, miR-150 and miR-223 were reported to be involved in adipogenesis ( 24 ), insulin resistance ( 25 , 26 ) and macrophage activation ( 27 ), while miR-130,miR-106b and miR-19b participate in cholesterol metabolism and efflux ( 14 ). The 5th quintile consisted of 125 miRNAs, including the 10% top expressed circulating miRNome with a log2 fold change (FC) greater than 5 (Supplementary Table 4).…”

Section: Resultsmentioning

confidence: 99%

Differences in circulating microRNA signature in Prader–Willi syndrome and non-syndromic obesity

Pascut

Tamini

Bresolin

et al. 2018

Endocrine Connections

View full text Add to dashboard Cite

Prader–Willi syndrome (PWS) represents the most common genetic-derived obesity disorder caused by the loss of expression of genes located on the paternal chromosome 15q11.2-q13. The PWS phenotype shows peculiar physical, endocrine and metabolic characteristics compared to those observed in non-syndromic essential obesity. Since miRNAs have now a well-established role in many molecular pathways, including regulatory networks related to obesity, this pilot study was aimed to characterize the expression of circulating miRNAs in PWS compared to essential obesity. The circulating miRNome of 10 PWS and 10 obese subjects, adequately matched for age, BMI and sex, was profiled throughout Genechip miRNA 4.0 microarray analysis. We identified 362 out of 2578 mature miRNAs to be expressed in serum of the studied population. The circulating miRNA signature significantly characterising the two populations include 34 differently expressed RNAs. Among them, miR-24-3p, miR-122 and miR-23a-3p highly differ between the two groups with a FC >10 in obese compared to PWS. In the obese subjects, miR-7107-5p, miR-6880-3p, miR-6793-3p and miR-4258 were associated to the presence of steatosis. A different signature of miRNAs significantly distinguished PWS with steatosis from PWS without steatosis, involving miR-619-5p, miR-4507, miR-4656, miR-7847-3p and miR-6782-5p. The miRNA target GO enrichment analysis showed the different pathway involved in these two different forms of obesity. Although the rarity of PWS actually represents a limitation to the availability of large series, the present study provides novel hints on the molecular pathogenesis of syndromic and non-syndromic obesity.

show abstract

Section: Resultsmentioning

confidence: 99%

Differences in circulating microRNA signature in Prader–Willi syndrome and non-syndromic obesity

Pascut

Tamini

Bresolin

et al. 2018

Endocrine Connections

View full text Add to dashboard Cite

show abstract

“…In addition, Rohm et al [60] found that the expression of hsa-let-7d-5p was increased in the experimental group compared with the undifferentiated control group during adipogenesis. Lozano-Bartolomé et al [61] showed that overexpression of miR-23a-3p was involved in insulin signaling in adipocytes in vitro. miR-27a-3p plays an important role in adipogenesis [62], regulation of fat function [63], increase in glycogen storage [64], and regulation of insulin sensitivity [65].…”

Section: Discussionmentioning

confidence: 99%

The Construction and Analysis of the Aberrant lncRNA-miRNA-mRNA Network in Adipose Tissue from Type 2 Diabetes Individuals with Obesity

Ding

Wang

et al. 2020

Journal of Diabetes Research

View full text Add to dashboard Cite

Background. The prevalence of obesity and type 2 diabetes mellitus (T2DM) has become the most serious global public health issue. In recent years, there has been increasing attention to the role of long noncoding RNAs (lncRNAs) in the occurrence and development of obesity and T2DM. The aim of this work was to find new lncRNAs as potential predictive biomarkers or therapeutic targets for obesity and T2DM. Methods. In this study, we identified significant differentially expressed mRNAs (DEmRNAs) and differentially expressed lncRNAs (DElncRNAs) between adipose tissue of individuals with obesity and T2DM and normal adipose tissue (absolute log 2 FC ≥ 1 and FDR < 0:05). Then, the lncRNA-miRNA interactions predicted by miRcode were further screened with a threshold of MIC > 0:2. Simultaneously, the mRNA-miRNA interactions were explored by miRWalk 2.0. Finally, a ceRNA network consisting of lncRNAs, miRNAs, and mRNAs was established by integrating lncRNA-miRNA interactions and mRNA-miRNA interactions. Results. Upon comparing adipose tissue from individuals with obesity and T2DM and normal adipose tissues, 364 significant DEmRNAs, including 140 upregulated and 224 downregulated mRNAs, were identified in GSE104674; in addition, 231 significant DEmRNAs, including 146 upregulated and 85 downregulated mRNAs, were identified in GSE133099. GO and KEGG analyses have shown that downregulated DEmRNAs in GSE104674 and GSE133099 were associated with obesity-and T2DM-related biological pathways, such as lipid metabolism, AMPK signaling, and insulin resistance. Furthermore, 28 significant DElncRNAs, including 14 upregulated and 14 downregulated lncRNAs, were found. Based on the predicted lncRNA-miRNA and mRNA-miRNA relationships, we constructed a competitive endogenous RNA (ceRNA) network, including five lncRNAs, ten miRNAs, and 15 mRNAs. KEGG-GSEA analysis revealed that four lncRNAs (FLG-AS1, SNAI3-AS1, AC008147.0, and LINC02015) in the ceRNA network were related to the biological pathways of metabolic diseases. Conclusions. Through ceRNA network analysis, our study identified four new lncRNAs that may be used as potential biomarkers and therapeutic targets of obesity and T2DM, thus laying a foundation for future clinical studies.

show abstract

“…Diet supplementation of l-cysteine increases PIP3 level and mediates the activation of PI3K, resulting in improvement of glucose metabolism [43,44]. Expression level of PTEN is also regulated epigenetically in adipocytes via several miRNAs such as miR-21, miR-23a-3p, miR-26a, miR-26b, and miR-181a-5p [45][46][47][48][49]. Another widely known PIP3 inhibitor is SHIP (SH2containing inositol 5′-phosphatase).…”

Section: Pi3k Kinase Subunitsmentioning

confidence: 99%

Role of PI3K/AKT Pathway in Insulin-Mediated Glucose Uptake

Świderska¹,

Strycharz²,

Wróblewski³

et al. 2020

Blood Glucose Levels

View full text Add to dashboard Cite

Glucose uptake is regulated by several mechanisms, where insulin plays the most prominent role. This powerful anabolic hormone regulates the transport of glucose into the cell through translocation of glucose transporter from an intracellular pool to the plasma membrane mainly in metabolically active tissues like skeletal muscles, adipose tissue, or liver (GLUT4). This translocation occurs through multiple steps of PI3K/AKT signaling pathway. In this chapter, we will focus on molecular events leading to GLUT4 translocation, starting with activation of insulin receptors through signaling cascade involving phosphatidylinositol 3-kinase (PI3K) and protein kinase B (PKB) and finally, the action of their effectors. We will present regulatory mechanisms and modulators of insulin-mediated glucose uptake.

show abstract

Altered Expression of miR-181a-5p and miR-23a-3p Is Associated With Obesity and TNFα-Induced Insulin Resistance

Abstract: miR-181a-5p and miR-23a-3p may prevent TNFα-induced IR in adipocytes through modulation of PTEN and S6K expression.

Cited by 72 publications

References 39 publications

Differences in circulating microRNA signature in Prader–Willi syndrome and non-syndromic obesity

Differences in circulating microRNA signature in Prader–Willi syndrome and non-syndromic obesity

The Construction and Analysis of the Aberrant lncRNA-miRNA-mRNA Network in Adipose Tissue from Type 2 Diabetes Individuals with Obesity

Role of PI3K/AKT Pathway in Insulin-Mediated Glucose Uptake

Contact Info

Product

Resources

About