LINE-1 methylation in visceral adipose tissue of severely obese individuals is associated with metabolic syndrome status and related phenotypes

Turcot, Valérie; Thewis, André; Deshaies, Yves; Pérusse, Louis; Bélisle, Alexandre; Marceau, Simon; Biron, Simon; Lescelleur, Odette; Biertho, Laurent; Vohl, Marie‐Claude

doi:10.1186/1868-7083-4-10

Cited by 66 publications

(59 citation statements)

References 54 publications

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“…Furthermore, recent studies have demonstrated a relationship between DNA methylation and metabolic diseases, such as obesity [21]. Therefore, the methylation levels of the promoter region in the following genes IL6 , LINE1 , SERPINE1, and TNF , previously linked with this type of pathological conditions [21,31,32,33,37,38,39], were evaluated in obese subjects with SAHS, in order to examine the molecular links between resting oxygen consumption and chronic diseases. Methylation levels of IL6 and SERPINE1 were positively associated with FFM.…”

Section: Discussionmentioning

confidence: 99%

“…Several polymerase chain reaction (PCR)-based methods have been used in order to easily analyze DNA methylation from leukocytes. In this context, global DNA methylation has been assessed measuring the methylation of CpG islands in the promoter region of the long interspersed nucleotide element 1 ( LINE1 ) retrotransposon [30,31,32,33], the only active, autonomous transposable element in humans [34]. Besides, some studies have investigated the relation between methylation pattern of genes with obesity, metabolic disturbances, and aging [27,28,35,36].…”

Section: Introductionmentioning

confidence: 99%

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Low Oxygen Consumption is Related to a Hypomethylation and an Increased Secretion of IL-6 in Obese Subjects with Sleep Apnea-Hypopnea Syndrome

Lopez‐Pascual

Lasa²,

Portillo³

et al. 2017

Ann Nutr Metab

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Background: Deoxyribonucleic acid (DNA) methylation is an epigenetic modification involved in gene expression regulation, usually via gene silencing, which contributes to the risks of many multifactorial diseases. The aim of the present study was to analyze the influence of resting oxygen consumption on global and gene DNA methylation as well as protein secretion of inflammatory markers in blood cells from obese subjects with sleep apnea-hypopnea syndrome (SAHS). Methods: A total of 44 obese participants with SAHS were categorized in 2 groups according to their resting oxygen consumption. DNA methylation levels were evaluated using a methylation-sensitive high resolution melting approach. Results: The analyzed interleukin 6 (IL6) gene cytosine phosphate guanine (CpG) islands showed a hypomethylation, while serum IL-6 was higher in the low compared to the high oxygen consumption group (p < 0.05). Moreover, an age-related loss of DNA methylation of tumor necrosis factor (B = -0.82, 95% CI -1.33 to -0.30) and long interspersed nucleotide element 1 (B = -0.46; 95% CI -0.87 to -0.04) gene CpGs were found. Finally, studied CpG methylation levels of serpin peptidase inhibitor, clade E member 1 (r = 0.43; p = 0.01), and IL6 (r = 0.41; p = 0.02) were positively associated with fat-free mass. Conclusions: These findings suggest a potential role of oxygen in the regulation of inflammatory genes. Oxygen consumption measurement at rest could be proposed as a clinical biomarker of metabolic health.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Low Oxygen Consumption is Related to a Hypomethylation and an Increased Secretion of IL-6 in Obese Subjects with Sleep Apnea-Hypopnea Syndrome

Lopez‐Pascual

Lasa²,

Portillo³

et al. 2017

Ann Nutr Metab

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“…Alterations of DNA methylation patterns have been associated with various diseases, including cancers and cardiovascular diseases (Wernimont et al, 2011;DelgadoCruzata et al, 2012). Lower global DNA methylation has been observed in individuals with severe metabolic syndrome (Turcot et al, 2012). Patients with vascular disease exhibit increased plasma total Hcy (tHcy) and decreased genomic DNA methylation (Castro et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Homocysteine induces blood vessel global hypomethylation mediated by LOX-1

Yang¹,

Tian²,

J³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Homocysteine (Hcy) is an independent risk factor of atherosclerosis through its involvement with the methionine cycle. In this study, we aimed to determine the blood vessel global methylation rate in Hcy-induced atherosclerosis in apolipoprotein-E-deficient (ApoE -/-) mice, and to explore the possible mechanism of this change in endothelial cells. ApoE -/-mice were divided into a hyperlipidemia (HLP) group, a hyperhomocysteinemia (HHcy) group, and an HHcy + folate + vitamin B12 (HHcy+FA+VB) group. Wild-type C57BL/6J mice were prepared as controls. Total Hcy, lipids, S-adenosylmethionine (SAM), and S-adenosylhomocysteine (SAH) contents in serum were measured with an automatic biochemistry analyzer and high-performance liquid chromatography. Methylation of B1 repetitive elements in blood vessels was tested using nested methylation-specific-polymerase chain reaction (nMS-PCR). Endothelial cells (ECs) were pretreated with Hcy or by adding FA and VB. Lectin-like oxidized LDL receptor-1 (LOX-1) expressions were determined by quantitative PCR, Western blot, and nMS-PCR. The HHcy group displayed severe HLP and HHcy. SAM and SAH contents were also elevated in the HHcy group compared with other groups. Methylation of B1 repetitive elements was significantly increased in the HHcy group (0.5050 ± 0.0182) compared to the HLP (0.5158 ± 0.0163) and control (0.5589 ± 0.0236) groups. mRNA and protein expressions of LOX-1 increased (0.2877 ± 0.0341, 0.6090 ± 0.0547), whereas methylation expression decreased (0.5527 ± 0.0148) after 100 µM Hcy stimulation in ECs. In conclusion, Hcy-induced atherosclerosis was closely associated with induced hypomethylation status in the blood vessel, and this process was partially mediated by LOX-1 DNA methylation.

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“…BMI and obesity have been associated with differential DNA methylation of immortalized lymphocytes and leukocytes, respectively [35,36]. Global DNA methylation, analyzed by measuring methylation of the repetitive LINE-1 element in visceral adipose tissue of obese subjects, was further associated with glucose levels and status of the metabolic syndrome [37]. Moreover, caloric restriction for 6 months induced epigenetic changes and coordinate changes in gene expression in adipose tissue of overweight and/or obese women [38].…”

Section: Non-genetic Risk Factors and Epigenetic Modifications In Tarmentioning

confidence: 99%

Epigenetic Modifications and Type 2 Diabetes in Humans

Ling¹

2014

Frontiers in Diabetes

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Type 2 diabetes (T2D) is a multifactorial, polygenic disease, and combinations of genetic and nongenetic factors contribute to its susceptibility. While obesity, physical inactivity and ageing represent non-genetic risk factors for T2D, approximately 60 common genetic variants are known to also increase the disease risk. Non-genetic risk factors may further interact with genetic factors, and thereby modulate the risk for T2D through gene-environment interactions. However, it is possible that the interaction between the genome and environment to modulate the risk for T2D also happens through direct chemical modifications of the genome by so-called epigenetic modifications. These epigenetic modifications include DNA methylation and histone modifications. Recent studies focusing on the role of epigenetics in the pathogenesis of T2D suggest that alterations in the DNA methylation pattern and histone modifications in target tissues for the disease, such as adipose tissue, skeletal muscle, pancreatic islets and liver, may contribute to the development of T2D. This chapter aims at summarizing some of the recent advances in the field of epigenetics and T2D.Although the genome of most cells in the human body has an identical nucleotide sequence, specific cell types and organs have different phenotypes. This may be due to epigenetic modifications that regulate cell-specific gene expression. Epigenetics has been defined as mitotically and/or meiotically heritable changes in gene function that occur without a change in the nucleotide sequence, and the epigenome includes DNA methylation, hydroxymethylation of DNA, histone modifications and possibly noncoding RNAs [1]. Epigenetic modifications do not only regulate cell-specific gene expression in differentiated cells, they are also used for X-chromosome inactivation, parental imprinting and for transcriptional regulation during embryonic development. Recent studies further show that epigenetic modifications regulate alternative splicing, alternative promoters and the recombination rate [2][3][4][5]. During recent years, there has been a growing interest in epigenetics, possibly because changes in the epi-

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LINE-1 methylation in visceral adipose tissue of severely obese individuals is associated with metabolic syndrome status and related phenotypes

Cited by 66 publications

References 54 publications

Low Oxygen Consumption is Related to a Hypomethylation and an Increased Secretion of IL-6 in Obese Subjects with Sleep Apnea-Hypopnea Syndrome

Low Oxygen Consumption is Related to a Hypomethylation and an Increased Secretion of IL-6 in Obese Subjects with Sleep Apnea-Hypopnea Syndrome

Homocysteine induces blood vessel global hypomethylation mediated by LOX-1

Epigenetic Modifications and Type 2 Diabetes in Humans

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