Obesity: genome and environment interactions

Bašić, Martina; Butorac, Ana; Jurčević, Irena Landeka; Bačun-Družina, Višnja

doi:10.2478/10004-1254-63-2012-2244

Cited by 19 publications

(27 citation statements)

References 94 publications

(80 reference statements)

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“…These anomalous global epigenetic changes may induce the obesogenic expression patterns [123]. Researchers also acknowledged the value of epigenetics that revealed plausible mechanism of environmental interaction that can set off disease state [124, 125]. …”

Section: Pcbs Exposures In Human and Early Disease Biomarkers: A Genomentioning

confidence: 99%

Biomarkers Linking PCB Exposure and Obesity.

Ghosh¹,

Murínová²,

Trnovec³

et al. 2014

CPB

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Recently the prevalence of obesity has increased dramatically across much of the world. Obesity, as a complex, multifactorial disease, and its health consequences probably result from the interplay of environmental, genetic, and behavioral factors. Several lines of evidence support the theory that obesity is programmed during early development and that environmental exposures can play a key role. We therefore hypothesize that the current epidemic might associated with the influence of chemical exposures upon genetically controlled developmental pathways, leading to metabolic disorders. Some environmental chemicals, such as PCBs and pesticide residues, are widespread in food, drinking water, soil, and they exert multiple effects including estrogenic on cellular processes; some have been shown to affect the development of obesity, insulin resistance, type 2 diabetes, and metabolic syndrome. To bring these lines of evidence together and address an important health problem, this narrative review has been primarily designed to address PCBs exposures that have linked with human disease, obesity in particular, and to assess the effects of PCBs on gene expression in a highly-exposed population. The results strongly suggest that further research into the specific mechanisms of PCBs-associated diseases is warranted.

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Section: Pcbs Exposures In Human and Early Disease Biomarkers: A Genomentioning

confidence: 99%

Biomarkers Linking PCB Exposure and Obesity.

Ghosh¹,

Murínová²,

Trnovec³

et al. 2014

CPB

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“…On the contrary, the association of GSTM1 deletion and molecular damage in atherosclerosis depends on different factors and includes other polymorphisms (gene-gene interactions), life style habits, and the influence of the environment (58,66). …”

Section: Interaction Of Other Atherosclerosis Risk Factors With Genetmentioning

confidence: 99%

“…Investigations aimed at the effect of the gene-smoking allow for a better understanding of gene-environment interactions. They should ultimately lead to the creation of a personalized medicine concept regarding cardiovascular diseases (58,66). …”

Section: Interaction Of Other Atherosclerosis Risk Factors With Genetmentioning

confidence: 99%

Polymorphisms of genes involved in polycyclic aromatic hydrocarbons’biotransformation and atherosclerosis

Marinković¹,

Pašalić

Potočki

2013

Biochem Med

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Polycyclic aromatic hydrocarbons (PAHs) are among the most prevalent environmental pollutants and result from the incomplete combustion of hydrocarbons (coal and gasoline, fossil fuel combustion, byproducts of industrial processing, natural emission, cigarette smoking, etc.). The first phase of xenobiotic biotransformation in the PAH metabolism includes activities of cytochrome P450 from the CYP1 family and microsomal epoxide hydrolase. The products of this biotransformation are reactive oxygen species that are transformed in the second phase through the formation of conjugates with glutathione, glucuronate or sulphates. PAH exposure may lead to PAH-DNA adduct formation or induce an inflammatory atherosclerotic plaque phenotype. Several genetic polymorphisms of genes encoded for enzymes involved in PAH biotransformation have been proven to lead to the development of diseases. Enzyme CYP P450 1A1, which is encoded by the CYP1A1 gene, is vital in the monooxygenation of lipofilic substrates, while GSTM1 and GSTT1 are the most abundant isophorms that conjugate and neutralize oxygen products. Some single nucleotide polymorphisms of the CYP1A1 gene as well as the deletion polymorphisms of GSTT1 and GSTM1 may alter the final specific cellular inflammatory respond. Occupational exposure or conditions from the living environment can contribute to the production of PAH metabolites with adverse effects on human health. The aim of this study was to obtain data on biotransformation and atherosclerosis, as well as data on the gene polymorphisms involved in biotransformation, in order to better study gene expression and further elucidate the interaction between genes and the environment.

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“…Accumulating evidence suggests that the interaction between stress exposure and diet imbalance can be an important connection between mood disorders and the global epidemic of obesity, but the mechanisms underlying this association are poorly understood (Basic et al, 2012; van Reedt Dortland et al, 2013; Blakemore and Buxton, 2014; Qi et al, 2014). Specific types of lipid contents in meals can stimulate the intestine–brain–liver neural axis that acts to regulate insulin sensitivity and circulating excess of nutrients (Wang et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Chronic psychological stress and high-fat high-fructose diet disrupt metabolic and inflammatory gene networks in the brain, liver, and gut and promote behavioral deficits in mice

Rodrigues

Bekhbat

Houser

et al. 2017

Brain, Behavior, and Immunity

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The mechanisms underlying the association between chronic psychological stress, development of metabolic syndrome (MetS), and behavioral impairment in obesity are poorly understood. The aim of the present study was to assess the effects of mild chronic psychological stress on metabolic, inflammatory, and behavioral profiles in a mouse model of diet-induced obesity. We hypothesized that (1) high-fat high-fructose diet (HFHF) and psychological stress would synergize to mediate the impact of inflammation on the central nervous system in the presence of behavioral dysfunction, and that (2) HFHF and stress interactions would impact insulin and lipid metabolism. C57Bl/6 male mice underwent a combination of HFHF and two weeks of chronic psychological stress. MetS-related conditions were assessed using untargeted plasma metabolomics, and structural and immune changes in the gut and liver were evaluated. Inflammation was measured in plasma, liver, gut, and brain. Our results show a complex interplay of diet and stress on gut alterations, energetic homeostasis, lipid metabolism, and plasma insulin levels. Psychological stress and HFHF diet promoted changes in intestinal tight junctions proteins and increases in insulin resistance and plasma cholesterol, and impacted the RNA expression of inflammatory factors in the hippocampus. Stress promoted an adaptive anti-inflammatory profile in the hippocampus that was abolished by diet treatment. HFHF increased hippocampal and hepatic Lcn2 mRNA expression as well as LCN2 plasma levels. Behavioral changes were associated with HFHF and stress. Collectively, these results suggest that diet and stress as pervasive factors exacerbate MetS-related conditions through an inflammatory mechanism that ultimately can impact behavior. This rodent model may prove useful for identification of possible biomarkers and therapeutic targets to treat metabolic syndrome and mood disorders.

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Obesity: genome and environment interactions

Cited by 19 publications

References 94 publications

Biomarkers Linking PCB Exposure and Obesity.

Biomarkers Linking PCB Exposure and Obesity.

Polymorphisms of genes involved in polycyclic aromatic hydrocarbons’biotransformation and atherosclerosis

Chronic psychological stress and high-fat high-fructose diet disrupt metabolic and inflammatory gene networks in the brain, liver, and gut and promote behavioral deficits in mice

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