A polymorphism in the Irisin-encoding gene (FNDC5) associates with hepatic steatosis by differential miRNA binding to the 3′UTR

Metwally, Mostafa; Bayoumi, Ali; Romero–Gómez, Manuel; Thabet, Khaled; John, Miya; Adams, Leon A.; Huo, Xiaoqi; Aller, R.; García‐Monzón, Carmelo; Arias-Loste, María Teresa; Bugianesi, Elisabetta; Miele, Luca; Gallego‐Durán, Rocío; Fischer, Janett; Berg, Thomas; Liddle, Christopher; Qiao, Liang; George, Jacob; Eslam, Mohammed

doi:10.1016/j.jhep.2018.10.021

Cited by 67 publications

(57 citation statements)

References 43 publications

(55 reference statements)

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“…This raises the question as to whether NAFLD-related sarcopenia is caused by myostatin activation in skeletal muscle, or sarcopenia is the primary abnormality related to myostatin, and consequently function in an endocrine manner thus activating fibrogenic hepatic stellate cells. Irisin, the cleaved extra-cellular fragment of the Fibronectin type III domain-containing protein 5 (FNDC5), another exercise-inducible myokine with favorable metabolic activity, is also involved in the control of energy expenditure, body weight, and regulation of insulin resistance (7,8). Recently an association among variants in the FNDC5 gene, in particular rs3480 (G) allele, and severe steatosis and fibrosis has emerged (8,9).…”

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confidence: 99%

“…Irisin, the cleaved extra-cellular fragment of the Fibronectin type III domain-containing protein 5 (FNDC5), another exercise-inducible myokine with favorable metabolic activity, is also involved in the control of energy expenditure, body weight, and regulation of insulin resistance (7,8). Recently an association among variants in the FNDC5 gene, in particular rs3480 (G) allele, and severe steatosis and fibrosis has emerged (8,9). Elevated serum irisin was moreover associated with reduced steatosis, and an improved metabolic profile (8).…”

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confidence: 99%

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Building mass to prevent non-alcoholic fatty liver disease?

Pelusi¹,

Valenti²

2019

Hepatobiliary Surg. Nutr

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confidence: 99%

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confidence: 99%

Building mass to prevent non-alcoholic fatty liver disease?

Pelusi¹,

Valenti²

2019

Hepatobiliary Surg. Nutr

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“…Based on the list, we searched NCBI dbSNP (http://www.ncbi.nlm.nih.gov/), HapMap (http://www.hapmap.org), and lncRNASNP (http://bioinfo.life.hust.edu.cn/lncRNASNP/) and identified 3765 SNPs. Considering that polymorphisms in the non‐coding regions may affect the binding of other transcripts such as microRNAs, we selected SNPs located in the binding sites which may alter the binding affinity of lncRNAs to other molecules. The following selection criteria were established to choose SNPs for genotyping: (a) minor allele frequency (MAF) reported in HapMap ≥5% in Chinese Han, Beijing (CHB); (b) located in the regulatory region of genes; and (c) affecting the binding with microRNAs.…”

Section: Methodsmentioning

confidence: 99%

SNPs in LncRNA genes are associated with non‐small cell lung cancer in a Chinese population

Wang

Feng

Wang

et al. 2019

Clinical Laboratory Analysis

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BackgroundIt has indicated that single nuclear polymorphisms (SNPs) in the regions encoding non‐coding transcripts are associated with lung cancer susceptibility. In a previous microarray study, we identified 13 differentially expressed long non‐coding RNAs (lncRNAs) in non‐small cell lung cancer (NSCLC) and associations of SNPs in these lncRNA genes with lung cancer were unknown. We conducted a case‐control study to address this issue.MethodsUsing the TaqMan method, we genotyped 17 SNPs located in the 13 lncRNA genes in 1294 cases with NSCLC and 1729 healthy controls. Unconditional logistic regression and Cox proportional hazards regression were used to analyze the associations of these SNPs with NSCLC risk and patient survival, respectively. These analyses were also repeated in subgroups of cases and controls stratified by gender, age group, smoking status, disease stage, and histological type.ResultsWe identified three SNPs associated with NSCLC risk. For SNP rs498238, CC genotype was associated with lower risk compared to TT genotype (adjusted OR = 0.33, 95%CI: 0.11‐0.97, P = 0.043). For rs16901995, CT/TT genotypes were associated with lower risk compared to CC genotype in non‐smokers (adjusted OR = 0.78, 95%CI: 0.62‐0.98, P = 0.035). Variant genotypes in rs219741 were associated with NSCLC risk in young patients, and the adjusted OR was 1.47 (95%CI: 1.03‐2.10, P = 0.033) when compared to the wild genotype. No SNPs were found to be associated with patient overall survival in the study.ConclusionThe study suggests that some genetic polymorphisms in the lncRNA genes may influence the risk of NSCLC among Chinese.

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“…The TM6SF2 E167 K variant is associated with a reduction in TM6SF2 activity, which leads to an increase in liver triglyceride content by decreasing VLDL secretion [ 28 ] and enhancing the expression of some genes associated with lipid metabolism, including PNPLA3, ACSS2, DGAT1, and DGAT2 [ 29 ], and the catalytic activities of sterol isomerases [ 30 ] as well as other still unidentified molecular pathways. Carriage of the FNDC5 rs3480 minor (G) allele was associated with more severe steatosis in NAFLD [ 31 ]. Investigations of biopsies from Caucasian women showed a strong association between SNP rs2645424 on chromosome 8 in the farnesyl diphosphate farnesyl transferase-1 gene ( FDFT-1 ) and nonalcoholic steatosis (NAS) [ 32 ].…”

Section: Genetics Of Nafldmentioning

confidence: 99%

Noncoding RNAs in Nonalcoholic Fatty Liver Disease: Potential Diagnosis and Prognosis Biomarkers

et al. 2020

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Nonalcoholic fatty liver disease (NAFLD) is currently the most common chronic liver disease worldwide in part due to the concomitant obesity pandemic and insulin resistance (IR). It is increasingly becoming evident that NAFLD is a disease affecting numerous extrahepatic vital organs and regulatory pathways. The molecular mechanisms underlying the nonalcoholic steatosis formation are poorly understood, and little information is available on the pathways that are responsible for the progressive hepatocellular damage that follows lipid accumulation. Recently, much research has focused on the identification of the epigenetic modifications that contribute to NAFLD pathogenesis. Noncoding RNAs (ncRNAs) are one of such epigenetic factors that could be implicated in the NAFLD development and progression. In this review, we summarize the current knowledge of the genetic and epigenetic factors potentially underlying the disease. Particular emphasis will be put on the contribution of microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs) to the pathophysiology of NAFLD as well as their potential use as therapeutic targets or as markers for the prediction and the progression of the disease.

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A polymorphism in the Irisin-encoding gene (FNDC5) associates with hepatic steatosis by differential miRNA binding to the 3′UTR

Cited by 67 publications

References 43 publications

Building mass to prevent non-alcoholic fatty liver disease?

Building mass to prevent non-alcoholic fatty liver disease?

SNPs in LncRNA genes are associated with non‐small cell lung cancer in a Chinese population

Noncoding RNAs in Nonalcoholic Fatty Liver Disease: Potential Diagnosis and Prognosis Biomarkers

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