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Association of polycyclic aromatic hydrocarbons with cardiometabolic risk factors and obesity in children.

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A limited body of evidence exists on the association of exposure to polycyclic aromatic hydrocarbons (PAHs) with cardiometabolic risk factors and obesity in children. No study has evaluated these associations in subgroups of children with and without excess weight, and those with and without

Pdgfrα-Cre mediated knockout of the aryl hydrocarbon receptor protects mice from high-fat diet induced obesity and hepatic steatosis

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Aryl hydrocarbon receptor (AHR) agonists such as dioxin have been associated with obesity and the development of diabetes. Whole-body Ahr knockout mice on high-fat diet (HFD) have been shown to resist obesity and hepatic steatosis. Tissue-specific knockout of Ahr in mature adipocytes via

Effects of Aryl Hydrocarbon Receptor Deficiency on PCB-77-Induced Impairment of Glucose Homeostasis during Weight Loss in Male and Female Obese Mice.

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Lipophilic polychlorinated biphenyls (PCBs) accumulate with obesity, but during weight loss, liberated PCBs act as ligands of the aryl hydrocarbon receptor (AhR) to negatively influence health. Previous studies demonstrated that PCB-77 administration to obese male mice impaired glucose

Obesity mediated the association of exposure to polycyclic aromatic hydrocarbon with risk of cardiovascular events.

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Exposure to polycyclic aromatic hydrocarbons (PAHs) could cause high blood pressure (BP) and increased risk for atherosclerotic cardiovascular disease (ASCVD). However, the mechanisms underlying the relationship between them were unclear. We investigated potential mediation effect of obesity on the

Exposure to polycyclic aromatic hydrocarbons and central obesity enhanced risk for diabetes among individuals with poor lung function.

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Some studies have shown an association between obesity or exposure to polycyclic aromatic hydrocarbons (PAHs) and the risk of diabetes. This study aimed to investigate the interaction of obesity and urinary monohydroxy-PAHs (OH-PAHs) on diabetes. Individuals (n = 2716) were drawn from the baseline

Potential role of aryl hydrocarbon receptor signaling in childhood obesity.

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There is a growing concern that junk food has contributed to the childhood obesity epidemic. Recently, experimental studies suggested that the aryl hydrocarbon receptor (AHR) gene is strongly linked to western diet-induced obesity.This study investigated

Synergistic interaction between polycyclic aromatic hydrocarbons and environmental tobacco smoke on the risk of obesity in children and adolescents: The U.S. National Health and Nutrition Examination Survey 2003-2008.

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BACKGROUND Polycyclic aromatic hydrocarbons (PAHs) may be obesogens. However, the role of PAHs independent of environmental tobacco smoke (ETS) is unclear, and the interaction between PAHs and ETS remains unknown. METHODS We performed cross-sectional analyses of urinary concentrations of PAH

Association of childhood obesity with maternal exposure to ambient air polycyclic aromatic hydrocarbons during pregnancy.

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There are concerns that prenatal exposure to endocrine-disrupting chemicals increases children's risk of obesity. African-American and Hispanic children born in the Bronx or Northern Manhattan, New York (1998-2006), whose mothers underwent personal air monitoring for polycyclic aromatic hydrocarbon

Polycyclic aromatic hydrocarbons in breast milk of obese vs normal women: Infant exposure and risk assessment.

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Biomonitoring of human breast milk is one of the best ways to identify body burdens of contaminants and associated risk estimation. The objectives of the current study were to evaluate milk concentrations of persistent organic pollutants (POPs), mainly polycyclic aromatic hydrocarbons (PAHs),

Hydrocarbons (jet fuel JP-8) induce epigenetic transgenerational inheritance of obesity, reproductive disease and sperm epimutations.

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Environmental compounds have been shown to promote epigenetic transgenerational inheritance of disease. The current study was designed to determine if a hydrocarbon mixture involving jet fuel (JP-8) promotes epigenetic transgenerational inheritance of disease. Gestating F0 generation female rats

Obesity is mediated by differential aryl hydrocarbon receptor signaling in mice fed a Western diet.

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BACKGROUND Obesity is a growing worldwide problem with genetic and environmental causes, and it is an underlying basis for many diseases. Studies have shown that the toxicant-activated aryl hydrocarbon receptor (AHR) may disrupt fat metabolism and contribute to obesity. The AHR is a nuclear

Obesity and fatty liver are prevented by inhibition of the aryl hydrocarbon receptor in both female and male mice.

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Inhibition of the aryl hydrocarbon receptor (AHR) prevents Western diet-induced obesity and fatty liver in C57Bl/6J (B6) male mice. The AHR is a ligand-activated nuclear receptor that regulates genes involved in xenobiotic metabolism and T-cell differentiation. Here, we tested the hypothesis that

Effects of Adipocyte Aryl Hydrocarbon Receptor Deficiency on PCB-Induced Disruption of Glucose Homeostasis in Lean and Obese Mice.

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BACKGROUND Coplanar polychlorinated biphenyls (PCBs) promote adipocyte inflammation and impair glucose homeostasis in lean mice. The diabetes-promoting effects of lipophilic PCBs have been observed only during weight loss in obese mice. The molecular mechanisms linking PCB exposures to impaired

Inhibition of the aryl hydrocarbon receptor prevents Western diet-induced obesity. Model for AHR activation by kynurenine via oxidized-LDL, TLR2/4, TGFβ, and IDO1.

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Obesity is an increasingly urgent global problem, yet, little is known about its causes and less is known how obesity can be effectively treated. We showed previously that the aryl hydrocarbon receptor (AHR) plays a role in the regulation of body mass in mice fed Western diet. The AHR is a

Polycyclic aromatic hydrocarbon exposure, obesity and childhood asthma in an urban cohort.

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BACKGROUND Exposure to traffic-related air pollutants, including polycyclic aromatic hydrocarbons (PAHs) from traffic emissions and other combustion sources, and childhood obesity, have been implicated as risk factors for developing asthma. However, the interaction between these two on asthma among

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