Altered intragenic DNA methylation of HOOK2 gene in adipose tissue from individuals with obesity and type 2 diabetes

Rodríguez-Rodero, Sandra; Torre, Edelmiro Menéndez; Fernández-Bayón, Gustavo; Sánchez, Paula Morales; Sanz, Lourdes; Santos, Estrella Olga Turienzo; González, Juan José; Martínez-Faedo, Ceferino; Suárez-Gutiérrez, Lorena; Blanco, Jessica Ares; Díaz-Naya, Lucia; Martín-Nieto, Alicia; Fernández-Morera, Juan Luís; Fraga, Mario F.; Delgado, Elías

doi:10.1371/journal.pone.0189153

Cited by 23 publications

(13 citation statements)

References 53 publications

(46 reference statements)

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“…HOOK2 belongs to the HOOK family of proteins, which are responsible for trafficking and anchoring of organelles in the cell through the binding and directing of microtubules [36]. A study of DNA methylation in adipose tissue from subjects with type II diabetes and obesity, using the 450K Illumina beadchip, identified HOOK2 as significantly differentially methylated from the healthy group, although their findings indicated that HOOK2 was hypermethylated while our results show the genes being hypomethylated [39]. In an additional DNA methylation study on mothers with gestational diabetes, HOOK2 was found to be commonly differentially methylated in the maternal blood, placenta, and umbilical cord [40].…”

Section: Regional Association Study (Dm)contrasting

confidence: 68%

Maternal diabetes and obesity influence the fetal epigenome in a largely Hispanic population

et al. 2020

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Background: Obesity and diabetes mellitus are directly implicated in many adverse health consequences in adults as well as in the offspring of obese and diabetic mothers. Hispanic Americans are particularly at risk for obesity, diabetes, and end-stage renal disease. Maternal obesity and/or diabetes through prenatal programming may alter the fetal epigenome increasing the risk of metabolic disease in their offspring. The aims of this study were to determine if maternal obesity or diabetes mellitus during pregnancy results in a change in infant methylation of CpG islands adjacent to targeted genes specific for obesity or diabetes disease pathways in a largely Hispanic population. Methods: Methylation levels in the cord blood of 69 newborns were determined using the Illumina Infinium MethylationEPIC BeadChip. Over 850,000 different probe sites were analyzed to determine whether maternal obesity and/or diabetes mellitus directly attributed to differential methylation; epigenome-wide and regional analyses were performed for significant CpG sites. Results: Following quality control, agranular leukocyte samples from 69 newborns (23 normal term (NT), 14 diabetes (DM), 23 obese (OB), 9 DM/OB) were analyzed for over 850,000 different probe sites. Contrasts between the NT, DM, OB, and DM/OB were considered. After correction for multiple testing, 15 CpGs showed differential methylation from the NT, associated with 10 differentially methylated genes between the diabetic and non-diabetic subgroups, CCDC110, KALRN, PAG1, GNRH1, SLC2A9, CSRP2BP, HIVEP1, RALGDS, DHX37, and SCNN1D. The effects of diabetes were partly mediated by the altered methylation of HOOK2, LCE3C, and TMEM63B. The effects of obesity were partly mediated by the differential methylation of LTF and DUSP22. Conclusions: The presented data highlights the associated altered methylation patterns potentially mediated by maternal diabetes and/or obesity. Larger studies are warranted to investigate the role of both the identified differentially methylated loci and the effects on newborn body composition and future health risk factors for metabolic disease. Additional future consideration should be targeted to the role of Hispanic inheritance. Potential future targeting of transgenerational propagation and developmental programming may reduce population obesity and diabetes risk.

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Section: Regional Association Study (Dm)contrasting

confidence: 68%

Maternal diabetes and obesity influence the fetal epigenome in a largely Hispanic population

et al. 2020

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“…This scenario is also rising in lower-middle-income nations, mostly in urban backgrounds. Overweight or obesity rates in Africa (1990–2014) increased by nearly double from 5.4 million to 10.6 million [ 11 ]. Overweight is mostly caused by the consumption of energy-dense foods when the ingestion of carbohydrates is higher than in a fat diet [ 12 ].…”

Section: Etiology Of Obesitymentioning

confidence: 99%

“…The search for genes that enhance the vulnerability to improve obesity has become progressively significant. There have been several studies that have proved that the candidate genes are extremely associated with obesity and elevated body weight [ 11 ].…”

Section: Etiology Of Obesitymentioning

confidence: 99%

Anti-Obesity Effects of Medicinal and Edible Mushrooms

Ganesan

2018

Molecules

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Obesity is a group of metabolic disorders caused by multiple factors, including heredity, diet, lifestyle, societal determinants, environment, and infectious agents, which can all lead to the enhancement of storage body fat. Excess visceral fat mass in adipose tissue generate several metabolic disorders, including cardiovascular diseases with chronic inflammation based pathophysiology. The objective of the current review is to summarize the cellular mechanisms of obesity that attenuate by antioxidant potentials of medicinal and edible mushrooms. Studies have showed that mushrooms potentially have antioxidant capacities, which increase the antioxidant defense systems in cells. They boost anti-inflammatory actions and thereby protect against obesity-related hypertension and dyslipidemia. The practice of regular consumption of mushrooms is effective in the treatment of metabolic syndrome, including obesity, and thus could be a good candidate for use in future pharmaceutical or nutraceutical applications.

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“…Rodriguez-Rodero et al . showed that a T2DM can lead to alterations in the methylation profile (especially hypomethylation) within the gene body 35 . Hypomethylated intron regions can give rise to alternative intragenic transcripts 36,37 .…”

Section: Discussionmentioning

confidence: 99%

Glomerular expression pattern of long non-coding RNAs in the type 2 diabetes mellitus BTBR mouse model

Reichelt-Wurm

Wirtz

Chittka

et al. 2019

Sci Rep

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The prevalence of type 2 diabetes mellitus (T2DM) and by association diabetic nephropathy (DN) will continuously increase in the next decades. Nevertheless, the underlying molecular mechanisms are largely unknown and studies on the role of new actors like long non-coding RNAs (lncRNAs) barely exist. In the present study, the inherently insulin-resistant mouse strain “black and tan, brachyuric” (BTBR) served as T2DM model. While wild-type mice do not exhibit pathological changes, leptin-deficient diabetic animals develop a severe T2DM accompanied by a DN, which closely resembles the human phenotype. We analyzed the glomerular expression of lncRNAs from wild-type and diabetic BTBR mice (four, eight, 16, and 24 weeks) applying the “GeneChip Mouse Whole Transcriptome 1.0 ST” array. This microarray covered more lncRNA gene loci than any other array before. Over the observed time, our data revealed differential expression patterns of 1746 lncRNAs, which markedly differed from mRNAs. We identified protein-coding and non-coding genes, that were not only co-located but also co-expressed, indicating a potentially cis-acting function of these lncRNAs. In vitro -experiments strongly suggested a cell-specific expression of these lncRNA-mRNA-pairs. Additionally, protein-coding genes, being associated with significantly regulated lncRNAs, were enriched in various biological processes and pathways, that were strongly linked to diabetes.

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Altered intragenic DNA methylation of HOOK2 gene in adipose tissue from individuals with obesity and type 2 diabetes

Cited by 23 publications

References 53 publications

Maternal diabetes and obesity influence the fetal epigenome in a largely Hispanic population

Maternal diabetes and obesity influence the fetal epigenome in a largely Hispanic population

Anti-Obesity Effects of Medicinal and Edible Mushrooms

Glomerular expression pattern of long non-coding RNAs in the type 2 diabetes mellitus BTBR mouse model

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