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MicroRNA, Insulin Resistance, and Metabolic Disorders
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MicroRNA, Insulin Resistance, and Metabolic Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 13225

Special Issue Editor

Prof. Dr. Wan Lee

E-Mail Website
Guest Editor
1. Department of Biochemistry, Dongguk University School of Medicine, Gyeongju 38066, Republic of Korea
2. Channelopathy Research Center (CRC), Dongguk University School of Medicine, Ilsan 10326, Republic of Korea
Interests: mechanotransduction; cytoskeleton remodeling; proliferation; differentiation; myogenesis; sarcopenia; insulin resistance; diabetes; metabolism; glucose metabolism; lipid metabolism; metabolic diseases; energy metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,  

Insulin resistance, characterized as inadequate insulin signal transduction within cells, is a major global health issue linked to various diseases, including type 2 diabetes, dyslipidemia, hypertension, and atherosclerosis. Over the last few decades, microRNAs (miRNAs) are becoming a hot topic in molecular and cellular biology as "key modulators" of physiological and pathophysiological processes. They can orchestrate cell-to-cell communication and mediate cellular processes in numerous ways by controlling gene expression at the transcriptional, post-transcriptional, and translational levels. Despite growing evidence that miRNAs play a significant prognostic and therapeutic role in insulin resistance and metabolic diseases, the precise mechanisms by which miRNAs lead to insulin resistance and metabolic disorders are unclear.

This Special Issue will discover the novel function and mechanism of miRNAs in the pathogenesis of insulin resistance and metabolic disorders in various tissues and organs. Additionally, this issue will discuss recent advances in the development and potential application of miRNAs as novel biomarkers and therapeutic targets for metabolic diseases. We encourage contributions of original research and review articles on all aspects of miRNAs associated with insulin resistance and metabolic disorders.

Prof. Dr. Wan Lee
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • MicroRNA
  • Insulin resistance
  • Metabolic diseases
  • Insulin signaling
  • Diabetes
  • Obesity

Published Papers (6 papers)

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Editorial

Jump to: Research, Review

3 pages, 189 KiB  
Editorial
MicroRNA, Insulin Resistance, and Metabolic Disorders
by Wan Lee
Int. J. Mol. Sci. 2022, 23(24), 16215; https://doi.org/10.3390/ijms232416215 - 19 Dec 2022
Cited by 4 | Viewed by 1258
Abstract
Insulin resistance is a significant health problem worldwide that contributes to a number of disorders, including type 2 diabetes and metabolic syndrome [...] Full article
(This article belongs to the Special Issue MicroRNA, Insulin Resistance, and Metabolic Disorders)

Research

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15 pages, 2542 KiB  
Article
miR-143-null Is against Diet-Induced Obesity by Promoting BAT Thermogenesis and Inhibiting WAT Adipogenesis
by Jie Liu, Jiatao Liu, Dewei Zeng, Huan Wang, Yun Wang, Jiali Xiong, Xingping Chen, Junyi Luo, Ting Chen, Qianyun Xi, Qingyan Jiang and Yongliang Zhang
Int. J. Mol. Sci. 2022, 23(21), 13058; https://doi.org/10.3390/ijms232113058 - 27 Oct 2022
Cited by 8 | Viewed by 1715
Abstract
Excessive energy intake is the main cause of obesity, and stimulation of brown adipose tissue (BAT) thermogenesis has emerged as an attractive tool for anti-obesity. Although miR-143 has been reported to promote white adipocyte differentiation, its role in BAT remains unclear. In our [...] Read more.
Excessive energy intake is the main cause of obesity, and stimulation of brown adipose tissue (BAT) thermogenesis has emerged as an attractive tool for anti-obesity. Although miR-143 has been reported to promote white adipocyte differentiation, its role in BAT remains unclear. In our study, we found that during HFD-induced obesity, the expression of miR-143 in BAT was significantly reduced, and the expression of miR-143 in WAT first increased and then decreased. Knockout (KO) of miR-143 with CRISPR/Cas9 did not affect the energy metabolism of normal diet fed mice and brown adipocyte differentiation but inhibited the differentiation of white adipocytes. Importantly, during high fat diet-induced obesity, miR-143KO significantly reduced body weight, and improved energy expenditure, insulin sensitivity, and glucose tolerance. Further exploration showed that miR-143KO reduced the weight of adipose tissue, promoted mitochondrial number and functions, induced thermogenesis and lipolysis of BAT, increased lipolysis, and inhibited lipogenesis of white adipose tissue (WAT). Our study considerably improves our collective understanding of the function of miR-143 in adipose tissue and its potential significance in anti-obesity and provides a new avenue for the management of obesity through the inhibition of miR-143 in BAT and WAT. Full article
(This article belongs to the Special Issue MicroRNA, Insulin Resistance, and Metabolic Disorders)
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18 pages, 2761 KiB  
Article
Implication of miR-155-5p and miR-143-3p in the Vascular Insulin Resistance and Instability of Human and Experimental Atherosclerotic Plaque
by Paula González-López, Carla Ares-Carral, Andrea R. López-Pastor, Jorge Infante-Menéndez, Tamara González Illaness, Melina Vega de Ceniga, Leticia Esparza, Nuria Beneit, José Luis Martín-Ventura, Óscar Escribano and Almudena Gómez-Hernández
Int. J. Mol. Sci. 2022, 23(18), 10253; https://doi.org/10.3390/ijms231810253 - 06 Sep 2022
Cited by 10 | Viewed by 2073
Abstract
(1) Background: Cardiovascular diseases (CVDs) are the main cause of death in developed countries, being atherosclerosis, a recurring process underlying their apparition. MicroRNAs (miRNAs) modulate the expression of their targets and have emerged as key players in CVDs; (2) Methods: 18 miRNAs were [...] Read more.
(1) Background: Cardiovascular diseases (CVDs) are the main cause of death in developed countries, being atherosclerosis, a recurring process underlying their apparition. MicroRNAs (miRNAs) modulate the expression of their targets and have emerged as key players in CVDs; (2) Methods: 18 miRNAs were selected (Pubmed and GEO database) for their possible role in promoting atherosclerosis and were analysed by RT-qPCR in the aorta from apolipoprotein E-deficient (ApoE−/−) mice. Afterwards, the altered miRNAs in the aorta from 18 weeks-ApoE−/− mice were studied in human aortic and carotid samples; (3) Results: miR-155-5p was overexpressed and miR-143-3p was downregulated in mouse and human atherosclerotic lesions. In addition, a significant decrease in protein kinase B (AKT), target of miR-155-5p, and an increase in insulin-like growth factor type II receptor (IGF-IIR), target of miR-143-3p, were noted in aortic roots from ApoE−/− mice and in carotid plaques from patients with advanced carotid atherosclerosis (ACA). Finally, the overexpression of miR-155-5p reduced AKT levels and its phosphorylation in vascular smooth muscle cells, while miR-143-3p overexpression decreased IGF-IIR reducing apoptosis in vascular cells; (4) Conclusions: Our results suggest that miR-155-5p and miR-143-3p may be implicated in insulin resistance and plaque instability by the modulation of their targets AKT and IGF-IIR, contributing to the progression of atherosclerosis. Full article
(This article belongs to the Special Issue MicroRNA, Insulin Resistance, and Metabolic Disorders)
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13 pages, 2101 KiB  
Article
MiR-183-5p Induced by Saturated Fatty Acids Hinders Insulin Signaling by Downregulating IRS-1 in Hepatocytes
by Mai Thi Nguyen, Kyung-Ho Min and Wan Lee
Int. J. Mol. Sci. 2022, 23(6), 2979; https://doi.org/10.3390/ijms23062979 - 10 Mar 2022
Cited by 3 | Viewed by 1796
Abstract
Excessive saturated fatty acids (SFA) uptake is known to be a primary cause of obesity, a widely acknowledged risk factor of insulin resistance and type 2 diabetes. Although specific microRNAs (miRNAs) targeting insulin signaling intermediates are dysregulated by SFA, their effects on insulin [...] Read more.
Excessive saturated fatty acids (SFA) uptake is known to be a primary cause of obesity, a widely acknowledged risk factor of insulin resistance and type 2 diabetes. Although specific microRNAs (miRNAs) targeting insulin signaling intermediates are dysregulated by SFA, their effects on insulin signaling and sensitivity are largely unknown. Here, we investigated the role of SFA-induced miR-183-5p in the regulation of proximal insulin signaling molecules and the development of hepatic insulin resistance. HepG2 hepatocytes treated with palmitate and the livers of high-fat diet (HFD)-fed mice exhibited impaired insulin signaling resulting from dramatic reductions in the protein expressions of insulin receptor (INSR) and insulin receptor substrate-1 (IRS-1). Differential expression analysis showed the level of miR-183-5p, which tentatively targets the 3′UTR of IRS-1, was significantly elevated in palmitate-treated HepG2 hepatocytes and the livers of HFD-fed mice. Dual-luciferase analysis showed miR-183-5p bound directly to the 3′UTR of IRS-1 and reduced IRS-1 expression at the post-transcriptional stage. Moreover, transfection of HepG2 hepatocytes with miR-183-5p mimic significantly inhibited IRS-1 expression and hindered insulin signaling, consequently inhibiting insulin-stimulated glycogen synthesis. Collectively, this study reveals a novel mechanism whereby miR-183-5p induction by SFA impairs insulin signaling and suggests miR-183-5p plays a crucial role in the pathogenesis of hepatic insulin resistance in the background of obesity. Full article
(This article belongs to the Special Issue MicroRNA, Insulin Resistance, and Metabolic Disorders)
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13 pages, 2363 KiB  
Article
Hyperglycemia Promotes Endothelial Cell Senescence through AQR/PLAU Signaling Axis
by Yiqi Wan, Zhirui Liu, Andong Wu, Abdul Haseeb Khan, Ying Zhu, Shuangjin Ding, Xueer Li, Ya Zhao, Ximo Dai, Jin Zhou, Jiankun Liu, Yuanyuan Li, Xueting Gong, Man Liu and Xiao-Li Tian
Int. J. Mol. Sci. 2022, 23(5), 2879; https://doi.org/10.3390/ijms23052879 - 07 Mar 2022
Cited by 18 | Viewed by 3420
Abstract
Hyperglycemia is reported to accelerate endothelial cell senescence that contributes to diabetic complications. The underlying mechanism, however, remains elusive. We previously demonstrated AQR as a susceptibility gene for type 2 diabetes mellitus (T2DM) and showed that it was increased in multiple tissues in [...] Read more.
Hyperglycemia is reported to accelerate endothelial cell senescence that contributes to diabetic complications. The underlying mechanism, however, remains elusive. We previously demonstrated AQR as a susceptibility gene for type 2 diabetes mellitus (T2DM) and showed that it was increased in multiple tissues in models with T2DM or metabolic syndrome. This study aimed to investigate the role of AQR in hyperglycemia-induced senescence and its underlying mechanism. Here, we retrieved several datasets of the aging models and found the expression of AQR was increased by high glucose and by aging across species, including C. elegans (whole-body), rat (cardiac tissues), and monkey (blood). we validated the increased AQR expression in senescent human umbilical vein endothelial cells (HUVECs). When overexpressed, AQR promoted the endothelial cell senescence, confirmed by an increased number of cells stained with senescence-associated beta-galactosidase and upregulation of CDKN1A (P21) as well as the prohibited cellular colony formation and G2/M phase arrest. To explore the mechanism by which AQR regulated the cellular senescence, transcriptomic analyses of HUVECs with the overexpression and knockdown of the AQR were performed. We identified 52 co-expressed genes that were enriched, in the terms of plasminogen activation, innate immunity, immunity, and antiviral defense. Among co-expressed genes, PLAU was selected to evaluate its contribution to senescence for its highest strength in the enrichment of the biological process. We demonstrated that the knockdown of PLAU rescued senescence-related phenotypes, endothelial cell activation, and inflammation in models induced by AQR or TNF-α. These findings, for the first time, indicate that AQR/PLAU is a critical signaling axis in the modulation of endothelial cell senescence, revealing a novel link between hyperglycemia and vascular dysfunction. The study may have implications in the prevention of premature vascular aging associated with T2DM. Full article
(This article belongs to the Special Issue MicroRNA, Insulin Resistance, and Metabolic Disorders)
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Review

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20 pages, 373 KiB  
Review
miRNAs as Biomarkers in Diabetes: Moving towards Precision Medicine
by Maria Alexandra Angelescu, Octavian Andronic, Simona Olimpia Dima, Irinel Popescu, Irit Meivar-Levy, Sarah Ferber and Daniela Lixandru
Int. J. Mol. Sci. 2022, 23(21), 12843; https://doi.org/10.3390/ijms232112843 - 25 Oct 2022
Cited by 13 | Viewed by 1851
Abstract
Diabetes mellitus (DM) is a complex metabolic disease with many specifically related complications. Early diagnosis of this disease could prevent the progression to overt disease and its related complications. There are several limitations to using existing biomarkers, and between 24% and 62% of [...] Read more.
Diabetes mellitus (DM) is a complex metabolic disease with many specifically related complications. Early diagnosis of this disease could prevent the progression to overt disease and its related complications. There are several limitations to using existing biomarkers, and between 24% and 62% of people with diabetes remain undiagnosed and untreated, suggesting a large gap in current diagnostic practices. Early detection of the percentage of insulin-producing cells preceding loss of function would allow for effective therapeutic interventions that could delay or slow down the onset of diabetes. MicroRNAs (miRNAs) could be used for early diagnosis, as well as for following the progression and the severity of the disease, due to the fact of their pancreatic specific expression and stability in various body fluids. Thus, many studies have focused on the identification and validation of such groups or “signatures of miRNAs” that may prove useful in diagnosing or treating patients. Here, we summarize the findings on miRNAs as biomarkers in diabetes and those associated with direct cellular reprogramming strategies, as well as the relevance of miRNAs that act as a bidirectional switch for cell therapy of damaged pancreatic tissue and the studies that have measured and tracked miRNAs as biomarkers in insulin resistance are addressed. Full article
(This article belongs to the Special Issue MicroRNA, Insulin Resistance, and Metabolic Disorders)
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