scholarly journals DNA methylation in the adipose tissue and whole blood of Agent Orange-exposed Operation Ranch Hand veterans: a pilot study

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Matthew R. Rytel ◽  
Rondi Butler ◽  
Melissa Eliot ◽  
Joseph M. Braun ◽  
E. Andres Houseman ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Adipose Tissue ◽  
Pilot Study ◽  
Air Force ◽  
Whole Blood ◽  
Body Burden ◽  
Serum Levels ◽  
Agent Orange ◽  
Health Study ◽  
The Impact

Abstract Background Between 1962 and 1971, the US Air Force sprayed Agent Orange across Vietnam, exposing many soldiers to this dioxin-containing herbicide. Several negative health outcomes have been linked to Agent Orange exposure, but data is lacking on the effects this chemical has on the genome. Therefore, we sought to characterize the impact of Agent Orange exposure on DNA methylation in the whole blood and adipose tissue of veterans enrolled in the Air Force Health Study (AFHS). Methods We received adipose tissue (n = 37) and whole blood (n = 42) from veterans in the AFHS. Study participants were grouped as having low, moderate, or high TCDD body burden based on their previously measured serum levels of dioxin. DNA methylation was assessed using the Illumina 450 K platform. Results Epigenome-wide analysis indicated that there were no FDR-significantly methylated CpGs in either tissue with TCDD burden. However, 3 CpGs in the adipose tissue (contained within SLC9A3, LYNX1, and TNRC18) were marginally significantly (q < 0.1) hypomethylated, and 1 CpG in whole blood (contained within PTPRN2) was marginally significantly (q < 0.1) hypermethylated with high TCDD burden. Analysis for differentially methylated DNA regions yielded SLC9A3, among other regions in adipose tissue, to be significantly differentially methylated with higher TCDD burden. Comparing whole blood data to a study of dioxin exposed adults from Alabama identified a CpG within the gene SMO that was hypomethylated with dioxin exposure in both studies. Conclusion We found limited evidence of dioxin associated DNA methylation in adipose tissue and whole blood in this pilot study of Vietnam War veterans. Nevertheless, loci in the genes of SLC9A3 in adipose tissue, and PTPRN2 and SMO in whole blood, should be included in future exposure analyses.

scholarly journals DNA Methylation in the Adipose Tissue and Whole Blood of Agent Orange-exposed Operation Ranch Hand Veterans

2020 ◽  
Author(s):  
Matthew Rae Rytel ◽  
Rondi Butler ◽  
Melissa Eliot ◽  
Joseph M. Braun ◽  
E. Andres Houseman ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Adipose Tissue ◽  
Vietnam War ◽  
Air Force ◽  
Whole Blood ◽  
Body Burden ◽  
Serum Levels ◽  
Agent Orange ◽  
Health Study ◽  
The Impact

Abstract BackgroundBetween 1962 and 1971, the US Air Force sprayed Agent Orange across Vietnam, exposing many soldiers to this dioxin-containing herbicide. Several negative health outcomes have been linked to Agent Orange exposure, but data is lacking on the effects this chemical has on the genome. Therefore, we sought to characterize the impact of Agent Orange exposure on DNA methylation in the whole blood and adipose tissue of veterans enrolled in the Air Force Health Study (AFHS). MethodsWe received adipose tissue (n=37) and whole blood (n=42) from veterans in the AFHS. Study participants were grouped as having low, moderate, or high TCDD body burden based on their previously measured serum levels of dioxin. DNA methylation was assessed using the Illumina 450K platform.ResultsEpigenome-wide analysis indicated that there were no FDR-significantly methylated CpGs in either tissue with TCDD burden. However, 3 CpGs in the adipose tissue (contained within SLC9A3, LYNX1, and TNRC18) were marginally significantly (q<0.1) hypomethylated, and 1 CpG in whole blood (contained within PTPRN2) was marginally significantly (q<0.1) hypermethylated with high TCDD burden. Analysis for differentially methylated DNA regions yielded SLC9A3, among other regions in adipose tissue, to be significantly differentially methylated with higher TCDD burden. Comparing whole blood data to a study of dioxin exposed adults from Alabama identified a CpG within the gene SMO that was hypomethylated with dioxin exposure in both studies. ConclusionWe found limited evidence of dioxin associated DNA methylation in adipose tissue and whole blood in this pilot study of Vietnam War veterans. Nevertheless, loci in the genes of SLC9A3 in adipose tissue, and PTPRN2 and SMO in whole blood, should be included in future exposure analyses.

The Impact of Exercise on DNA Methylation of Genes Associated with Type 2 Diabetes and Obesity in Human Adipose Tissue

2014 ◽  
Vol 10 (01) ◽  
pp. 64 ◽  
Author(s):  
Tina Rönn ◽  
Charlotte Ling ◽  
◽  
Keyword(s):  
Type 2 Diabetes ◽  
Dna Methylation ◽  
Adipose Tissue ◽  
Human Adipose Tissue ◽  
Short Review ◽  
Methylation Pattern ◽  
Cellular Level ◽  
Genetic And Environmental Factors ◽  
The Impact

It is well established that exercise promotes health, and reduces people’s risks for developing type 2 diabetes and becoming obese. But just how exercise performs this, at a cellular level, and what molecular and physiologic steps are involved and in what order, are still not fully understood. Metabolic disorders are often influenced by interactions between genetic and environmental factors. One possible explanation for how the environment may influence the genome is through epigenetic mechanisms–that is–chemical modifications to the DNA itself. Epigenetic factors include, for example, DNA methylation, histone modifications, and different RNA-mediated processes, which all have the ability to bind to DNA or affect the chromatin structure and thereby change how specific genes are interpreted and expressed. In this short review, we focus on describing how exercise influences the genome-wide DNA methylation pattern, including candidate genes for obesity and type 2 diabetes, in human adipose tissue.

The Impact of Arsenic Exposure on Whole Blood DNA Methylation: An Epigenome-Wide Study of Bangladeshi Adults

2018 ◽  
Vol 2018 (1) ◽  
Author(s):  
Kathryn Demanelis ◽  
Maria Argos ◽  
Lin Tong ◽  
Justin Shinkle ◽  
Mekala Sabarinathan ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Whole Blood ◽  
Arsenic Exposure ◽  
Impact Of Arsenic ◽  
The Impact

scholarly journals Sex-specific Relationships Between Il-3, Il-7 and Lipids in African Americans

2020 ◽  
Author(s):  
Ariel Williams ◽  
Catherine Wooten ◽  
Quantil Melendez ◽  
Natasha Greene ◽  
Dayami Lopez ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
African Americans ◽  
Immune Responses ◽  
Sex Chromosome ◽  
Serum Levels ◽  
Serum Samples ◽  
Chronic Disorder ◽  
High Hba1c ◽  
Visceral Adipose ◽  
The Impact

Abstract Purpose: Obesity, a complex chronic disorder characterized by the enlargement of adipose tissue, has a multifactorial etiology. Adipose tissue is now recognized as an active tissue in the regulation of inflammation. Sex chromosome genes and hormones influences immune responses between males and females. Inflammation is rampant in obesity due to the expansion of visceral adipose tissue leading to insulin resistance resulting in type-2 diabetes (T2D). Differences in sex may lead to varied immune responses to T2D.Methods: A total of 116 serum samples were collected from African Americans: 68 women and 48 men. All participants had a BMI > 30. This group consists of 49 normal HbA1c and 71 high HbA1c participants. This study was designed to determine the impact of current circulating glucose on current serum IL-3 and IL-7 levels.Results:Serum cytokine levels are influenced by circulating high glucose and it varies based on sex. We found in women, IL-3 and IL-7 levels were upregulated 1.7-fold in the presence of high circulating glucose. In men, IL-3 levels were downregulated 1.5-fold and IL-7 levels downregulated 1.3-fold in the presence of high circulating glucose. IL-3 and IL-7 serum levels are also correlated with several lipid parameters.Conclusion: IL-3 and IL-7 are members of a complex network of cytokines that play a role in chronic inflammation. Inflammatory signaling impact several diseases including obesity, T2D, atherosclerosis and dyslipidemia. A better understanding of the pathological signaling of cytokines will help facilitate our understanding of inflammation in these diseases.

DNA methylation of the Klf14 gene region in whole blood cells provides prediction for the chronic inflammation in the adipose tissue

2018 ◽  
Vol 497 (3) ◽  
pp. 908-915 ◽  
Author(s):  
Chihiro Iwaya ◽  
Hidetoshi Kitajima ◽  
Ken Yamamoto ◽  
Yasutaka Maeda ◽  
Noriyuki Sonoda ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Adipose Tissue ◽  
Chronic Inflammation ◽  
Whole Blood ◽  
Blood Cells ◽  
Gene Region ◽  
Whole Blood Cells

scholarly journals Altered Blood Levels of Vitamin D, Cathelicidin and Parathyroid Hormone in Patients with Sepsis—a Pilot Study

2017 ◽  
Vol 45 (1) ◽  
pp. 36-45 ◽  
Author(s):  
T. Greulich ◽  
W. Regner ◽  
M. Branscheidt ◽  
C. Herr ◽  
A. R. Koczulla ◽  
...  
Keyword(s):  
Vitamin D ◽  
Antimicrobial Activity ◽  
Parathyroid Hormone ◽  
Pilot Study ◽  
Serum Levels ◽  
Blood Levels ◽  
Healthy Controls ◽  
Icu Patients ◽  
The Impact

It has been recognised that vitamin D (VitD) has a potential role in the regulation of inflammation and protection from infection. In a prospective clinical observational pilot study, we investigated the serum levels of 25-hydroxyvitamin-D3 (25(OH D3), 1,25-hydroxyvitamin-D3 (1,25(OH)2D3), parathyroid hormone (PTH), and cathelicidin in intensive care unit (ICU) patients with or without systemic inflammatory response syndrome (SIRS). We included 32 patients with SIRS (septic patients), 16 ICU patients without SIRS, and 16 healthy controls. To substantiate the findings of the clinical study, we stimulated monocyte-derived macrophages with microbial patterns and analysed the impact of VitD on release of cytokines and antimicrobial activity. We found that patients with or without SIRS had relatively low levels of 25(OH)D3 and 1,25(OH)2D3. Patients with sepsis had significantly lower levels of 25(OH)D3 as compared to ICU control patients and healthy controls (10.53 ± 11.3 μg/l versus 16.46 ± 12.58 μg/l versus 24.04 ± 12.07 μg/l); the same was true for 1,25(OH)2D3. Serum levels of PTH and cathelicidin were significantly increased in sepsis patients, as compared to the other groups. In vitro, VitD significantly decreased the release of pro-inflammatory cytokines from macrophages and increased the antimicrobial activity of the cells. We concluded that patients with sepsis have significantly lower VitD levels. In vitro, VitD modulates inflammation and increases the antibacterial activity of innate immune cells. These findings suggest that VitD insufficiency is mechanistically related to increased susceptibility to SIRS and sepsis.

scholarly journals Adipose Tissue Epigenetic Profile in Obesity-Related Dysglycemia - A Systematic Review

2021 ◽  
Vol 12 ◽  
Author(s):  
Sara Andrade ◽  
Tiago Morais ◽  
Ionel Sandovici ◽  
Alexandre L. Seabra ◽  
Miguel Constância ◽  
...  
Keyword(s):  
Systematic Review ◽  
Dna Methylation ◽  
Adipose Tissue ◽  
Whole Blood ◽  
Intracellular Signaling ◽  
Phenotypic Variability ◽  
Normal Weight ◽  
Small Gtpases ◽  
Metabolic Complications ◽  
Epigenetic Marks

BackgroundObesity is a major risk factor for dysglycemic disorders, including type 2 diabetes (T2D). However, there is wide phenotypic variation in metabolic profiles. Tissue-specific epigenetic modifications could be partially accountable for the observed phenotypic variability.ScopeThe aim of this systematic review was to summarize the available data on epigenetic signatures in human adipose tissue (AT) that characterize overweight or obesity-related insulin resistance (IR) and dysglycemia states and to identify potential underlying mechanisms through the use of unbiased bioinformatics approaches.MethodsOriginal data published in the last decade concerning the comparison of epigenetic marks in human AT of individuals with metabolically unhealthy overweight/obesity (MUHO) versus normal weight individuals or individuals with metabolically healthy overweight/obesity (MHO) was assessed. Furthermore, association of these epigenetic marks with IR/dysglycemic traits, including T2D, was compiled.ResultsWe catalogued more than two thousand differentially methylated regions (DMRs; above the cut-off of 5%) in the AT of individuals with MUHO compared to individuals with MHO. These DNA methylation changes were less likely to occur around the promoter regions and were enriched at loci implicated in intracellular signaling (signal transduction mediated by small GTPases, ERK1/2 signaling and intracellular trafficking). We also identified a network of seven transcription factors that may play an important role in targeting DNA methylation changes to specific genes in the AT of subjects with MUHO, contributing to the pathogeny of obesity-related IR/T2D. Furthermore, we found differentially methylated CpG sites at 8 genes that were present in AT and whole blood, suggesting that DMRs in whole blood could be potentially used as accessible biomarkers of MUHO.ConclusionsThe overall evidence linking epigenetic alterations in key tissues such AT to metabolic complications in human obesity is still very limited, highlighting the need for further studies, particularly those focusing on epigenetic marks other than DNA methylation. Our initial analysis suggests that DNA methylation patterns can potentially discriminate between MUHO from MHO and provide new clues into why some people with obesity are less susceptible to dysglycemia. Identifying AT-specific epigenetic targets could also lead to novel approaches to modify the progression of individuals with obesity towards metabolic disease.Systematic Review RegistrationPROSPERO, identifier CRD42021227237.

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