Epigenetics: A Molecular Link Between Environmental Factors and Type 2 Diabetes

Department of Clinical Sciences, Lund University Diabetes Center, Lund University, Malmö, Sweden.
Diabetes (Impact Factor: 8.1). 12/2009; 58(12):2718-25. DOI: 10.2337/db09-1003
Source: PubMed
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    • "Protein demethylase KDM3A is coupled to the regulation of genes involved in beta-adrenergic stimulated glycerol release and fatty acid oxidation such as uncoupling protein 1 (UCP1) (Tateishi et al., 2009). Extensive correlation between epigenetics and abnormal metabolic state have been noted in metabolic diseases such as obesity (Campion et al., 2009) and type 2 diabetes (Campion et al., 2009; Ling and Groop, 2009). There has been substantial evidence for the idea that the prevalence of OA is positively correlated with that of metabolic syndrome (Table 1) (Kornaat et al., 2009; Puenpatom and Victor, 2009; Zhuo et al., 2012). "
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    ABSTRACT: Osteoarthritis (OA) is one of the most prevalent forms of joint disorder, associated with a tremendous socioeconomic burden worldwide. Various non-genetic and lifestyle-related factors such as aging and obesity have been recognized as major risk factors for OA, underscoring the potential role for epigenetic regulation in the pathogenesis of the disease. OA-associated epigenetic aberrations have been noted at the level of DNA methylation and histone modification in chondrocytes. These epigenetic regulations are implicated in driving an imbalance between the expression of catabolic and anabolic factors, leading eventually to osteoarthritic cartilage destruction. Cellular senescence and metabolic abnormalities driven by OAassociated risk factors appear to accompany epigenetic drifts in chondrocytes. Notably, molecular events associated with metabolic disorders influence epigenetic regulation in chondrocytes, supporting the notion that OA is a metabolic disease. Here, we review accumulating evidence supporting a role for epigenetics in the regulation of cartilage homeostasis and OA pathogenesis.
    Moleculer Cells 08/2015; 38(8). DOI:10.14348/molcells.2015.0200 · 2.09 Impact Factor
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    • "Genetic predisposition while undoubtedly important is not the sole determinant of T2DM development, raising the collective importance of factors including diet and the environment in the genesis of T2DM (Noble et al., 2011; Talmud et al., 2010). It is possible that familial clustering of T2DM may have little to do with genetics, but may simply reflect shared environmental risk factors (eg sedentary lifestyle, pollutant exposures and gut flora to name a few) (Adamo and Tesson, 2008; Ling and Groop, 2009). While a number of factors such as obesity, sedentary lifestyle, stress, unhealthy diet, and smoking have been persuasively demonstrated to contribute to the pathogenesis of T2DM, the role of factors in the physical environment (ie air and water pollution, noise, disruptions in sleep-wake cycle owing to pervasive exposure to light at night-time) has not received much attention. "
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    ABSTRACT: Recent studies in both humans and animals suggest that air pollution is an important risk factor for type 2 diabetes mellitus (T2DM). However, the mechanism by which air pollution mediates propensity to diabetes is not fully understood. While a number of epidemiologic studies have shown a positive association between ambient air pollution exposure and risk for T2DM, some studies have not found such a relationship. Experimental studies in susceptible disease models do support this association and suggest the involvement of tissues involved in the pathogenesis of T2DM such as the immune system, adipose, liver, and central nervous system. This review summarizes the epidemiologic and experimental evidence between ambient outdoor air pollution and T2DM. © The Author 2015. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail:
    Toxicological Sciences 02/2015; 143(2):231-41. DOI:10.1093/toxsci/kfu250 · 3.85 Impact Factor
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    • "Like any complex phenotype, the epigenetic control of gene expression activity can be influenced by both genetic and environmental factors. In fact, recent research showed that the impact of the environment can be acquired via the epigenome (Fraga et al., 2005; Wong et al., 2005; Poulsen et al., 2007; Szyf et al., 2008; Ling and Groop, 2009), a hot area in complex disease studies including cancer that draws active research. With the rapid development in epigenomic analysis using next-generation sequencing or array-based technologies, the newly emerging epigenetic epidemiology is serving as a bridge linking gene activity with environmental conditions. "
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    ABSTRACT: Since the final decades of the last century, twin studies have made a remarkable contribution to the genetics of human complex traits and diseases. With the recent rapid development in modern biotechnology of high-throughput genetic and genomic analyses, twin modelling is expanding from analysis of diseases to molecular phenotypes in functional genomics especially in epigenetics, a thriving field of research that concerns the environmental regulation of gene expression through DNA methylation, histone modification, microRNA and long non-coding RNA expression, etc. The application of the twin method to molecular phenotypes offers new opportunities to study the genetic (nature) and environmental (nurture) contributions to epigenetic regulation of gene activity during developmental, ageing and disease processes. Besides the classical twin model, the case co-twin design using identical twins discordant for a trait or disease is becoming a popular and powerful design for epigenome-wide association study in linking environmental exposure to differential epigenetic regulation and to disease status while controlling for individual genetic make-up. It can be expected that novel uses of twin methods in epigenetic studies are going to help with efficiently unravelling the genetic and environmental basis of epigenomics in human complex diseases. © 2015. Published by The Company of Biologists Ltd.
    Journal of Experimental Biology 01/2015; 218(Pt 1):134-139. DOI:10.1242/jeb.107151 · 2.90 Impact Factor
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