Integrated analysis of long noncoding RNA and mRNA expression profile in children with obesity by microarray analysis

Liu, Yuesheng; Ji, Yibing; Li, Min; Wang, Min; Yi, Xiaoqing; Chen, Yin; Wang, Sisi; Zhang, Meizhen; Zhao, Zhao; Xiao, Yanfeng

doi:10.1038/s41598-018-27113-w

Cited by 40 publications

(44 citation statements)

References 46 publications

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“…Supporting the present data, previous studies have reported the induction of several lncRNAs in adipose tissue and targeting the main transcription factors of lipogenesis and adipogenesis, including PPARγ and SREBP-1 [11,[37][38][39][40][41]. For instance, knockdown of RP11-20G13.3 significantly decreased expression of markers of adipocyte differentiation: PPARγ, C/EBPα, and adiponectin [14]. Moreover, correlation analysis demonstrated that lncRNA RP11-20G13.3 in adipose tissue from obese and non-obese children was positively associated with obesity indices, circulating levels of insulin, LDL-C,and hs-CRP [14].…”

Section: Discussionsupporting

confidence: 88%

“…For instance, knockdown of RP11-20G13.3 significantly decreased expression of markers of adipocyte differentiation: PPARγ, C/EBPα, and adiponectin [14]. Moreover, correlation analysis demonstrated that lncRNA RP11-20G13.3 in adipose tissue from obese and non-obese children was positively associated with obesity indices, circulating levels of insulin, LDL-C,and hs-CRP [14].…”

Section: Discussionmentioning

confidence: 97%

“…The differential expression of several lncRNAs (e.g. RP11-20G13.3, HOTAIR,GYG2P1, and OLMALINC) has been shown in adipose tissue from both obese and non-obese subjects [14,34]. Moreover, the contribution Table 3 Unadjusted and adjusted correlation of MALAT1 gene expression in SAT and VAT of the whole population study with anthropometric and metabolic profiles BMI, body mass index; WC, waist circumference; WHR, waist-to-hip ratio; FBG, fasting blood glucose; HDL-high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; TC, total cholesterol; TG, triglycerides; hs-CRP, high-sensitivity C-reactive Protein; HOMA-IR, homeostasis model assessment of insulin resistance; eGFR, estimated glomerular filtration rate a Correlation is significant at the 0.05 level (2-tailed) of lncRNAs in the field of obesity-related research has been validated in in vitro and animal models more than in specific human tissues [35][36][37].…”

Section: Discussionmentioning

confidence: 99%

“…In another study, the knockdown of adipocyte-specific metabolic-related lncRNAs (ASMERs) in differentiated human adipocytes showed that ASMERs may be possible modulators of adipogenesis, lipid mobilization, and adiponectin expression [13]. Integrated analysis of LncRNA profiles in obese children revealed that hub lncRNA RP11-20G13.3 suppressed adipogenesis [14].…”

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confidence: 99%

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Adipose tissue gene expression of long non-coding RNAs; MALAT1, TUG1 in obesity: is it associated with metabolic profile and lipid homeostasis-related genes expression?

Ebrahimi

Toolabi

Pour

et al. 2020

Diabetol Metab Syndr

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Background: Recent studies point toward the possible regulatory roles of two lncRNAs; metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and taurine upregulated gene 1 (TUG1) in the pathogenesis of obesity-related disorders and regulation of lipogenesis and adipogenesis. In an attempt to understand the molecules involved in human obesity pathogenesis, we aimed to evaluate the expression of MALAT1 and TUG1 in visceral adipose tissues (VAT) and subcutaneous adipose tissues (SAT) of obese women, as compared to normal-weight women. The mRNA expression of possible target genes including peroxisome proliferator-activated receptor gamma (PPARγ), PPARγ coactivator-1 alpha (PGC1α), sterol regulatory element-binding protein-1c (SREBP-1c), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC) which are involved in adipogenesis and lipogenesis were also examined. Methods: This study was conducted on 20 obese [body mass index (BMI) ≥ 30 kg/m 2] female participants and 19 normal-weight (BMI < 25 kg/m 2) female participants. Real-time PCR was performed to investigate the mRNA expression of the above-mentioned genes in VAT and SAT from all participants. Results: The results showed lower mRNA levels of TUG1 in both the VAT and SAT of obese women, compared to normal-weight women. Furthermore, TUG1 expression in SAT positively correlated with BMI, waist circumference (WC), hip circumference, HOMA-IR, and insulin levels, eGFR value, creatinine levels, and hs-CRP in all participants independent of age and HOMA-IR. However, VAT mRNA expression of TUG1 had a positive correlation with obesity indices and HOMA-IR and insulin levels in the whole population. Moreover, SAT mRNA level of TUG1 was positively correlated with SAT gene expression of PGC1α, SREBP-1c, FAS, and ACC independent of age and HOMA-IR. Although mRNA expression of MALAT1 did not differ between two groups for any tissue, it was positively correlated with SAT mRNA levels of SREBP-1c, PPARγ, and their targets; FAS and ACC, as well as with VAT mRNA levels of PGC1α. Conclusions: It seems likely that TUG1 with distinct expression pattern in VAT and SAT are involved in the regulation of lipogenic and adipogenic genes and obesity-related parameters. However, more studies are necessary to establish this concept.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Adipose tissue gene expression of long non-coding RNAs; MALAT1, TUG1 in obesity: is it associated with metabolic profile and lipid homeostasis-related genes expression?

Ebrahimi

Toolabi

Pour

et al. 2020

Diabetol Metab Syndr

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“…Other lncRNAs, such as U90926, MIR221HG, and RP11-20G13. 3, have also been shown to be negatively related to adipogenesis (101)(102)(103). These studies indicate that lncRNAs regulate white adipogenesis through lncRNA-protein, lncRNA-mRNA, and lncRNA-miRNA interactions.…”

Section: Role Of Lncrnas In White Adipocyte Adipogenesismentioning

confidence: 79%

Regulation of Glucose and Lipid Metabolism by Long Non-coding RNAs: Facts and Research Progress

et al. 2020

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Long non-coding RNAs (lncRNAs) are a type of non-coding RNA with a length that exceeds 200 nucleotides. Previous studies have shown that lncRNAs play an important role in the pathogenesis of various diseases. Research in both animal models and humans has begun to unravel the profound complexity of lncRNAs and demonstrated that lncRNAs exert direct effects on glucose and lipid metabolism both in vivo and in vitro. Such research has elucidated the regulatory role of lncRNAs in glucose and lipid metabolism in human disease. lncRNAs mediate glucose and lipid metabolism under physiological and pathological conditions and contribute to various metabolism disorders. This review provides an update on our understanding of the regulatory role of lncRNAs in glucose and lipid metabolism in various diseases. As our understanding of the function of lncRNAs improves, the future is promising for the development of new diagnostic biomarkers that utilize lncRNAs and treatments that target lncRNAs to improve clinical outcomes.

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TNF‐α Upregulates IKKε Expression via the Lin28B/let‐7a Pathway to Induce Catecholamine Resistance in Adipocytes

Wang

Liu

et al. 2019

Obesity

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Objective Overexpression of inhibitor of nuclear factor kappa‐B kinase subunit epsilon (IKKε) contributes to blunted catecholamine‐induced lipolysis. Tumor necrosis factor α (TNF‐α) upregulates adipose IKKε expression to inhibit stimulated lipolysis, which can be reversed by IKKε inhibitors. This study investigated adipose IKKε expression in children with and without obesity and potential involvement of the Lin28B/let‐7a axis in posttranscriptional regulation of TNF‐α‐stimulated IKKε in adipocytes. Methods Adipose IKKε was detected in children both with and without obesity. The effects of TNF‐α on IKKε expression of adipocytes were investigated. Inhibitor and mimics of microRNA let‐7a or short interfering RNA of protein lin‐28 homolog B (Lin28B) were used to determine the effect of the Lin28B/let‐7a axis on TNF‐α‐mediated IKKε upregulation. Reporter assays were performed to confirm that let‐7a targets the IKKε gene. Results Adipose IKKε expression in children with obesity was upregulated to a greater extent than that in children without obesity and was positively correlated with BMI. TNF‐α increased IKKε expression through activation of Lin28B/let‐7a and then inhibited isoproterenol‐stimulated lipolysis in adipocytes. Blocking the Lin28B /let‐7a axis rescued inhibition of isoproterenol‐stimulated lipolysis produced by TNF‐α by inhibiting IKKε expression. Reporter assays confirmed that IKKε is a target of let‐7a. Conclusions Adipose IKKε expression in children with obesity is substantially elevated and positively correlated with BMI. TNF‐α induces catecholamine resistance via activation of the Lin28B/let‐7a/IKKε pathway.

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Integrated analysis of long noncoding RNA and mRNA expression profile in children with obesity by microarray analysis

Cited by 40 publications

References 46 publications

Adipose tissue gene expression of long non-coding RNAs; MALAT1, TUG1 in obesity: is it associated with metabolic profile and lipid homeostasis-related genes expression?

Adipose tissue gene expression of long non-coding RNAs; MALAT1, TUG1 in obesity: is it associated with metabolic profile and lipid homeostasis-related genes expression?

Regulation of Glucose and Lipid Metabolism by Long Non-coding RNAs: Facts and Research Progress

TNF‐α Upregulates IKKε Expression via the Lin28B/let‐7a Pathway to Induce Catecholamine Resistance in Adipocytes

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