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
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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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    • "In addition, T2D develops when cells fail to compensate for the increasing demand for insulin caused by insulin resistance (Saisho 2015). T2D is a complex disease that results from interactions of genetic, epigenetic and non-genetic factors (Ling and Groop 2009). The aim of this review is to summarize current research covering the role of epigenetic dysregulation of pancreatic islets in impaired insulin secretion and T2D. "
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    ABSTRACT: β cell dysfunction is central to the development and progression of type 2 diabetes (T2D). T2D develops when β cells are not able to compensate for the increasing demand for insulin caused by insulin resistance. Epigenetic modifications play an important role in establishing and maintaining β cell identity and function in physiological conditions. On the other hand, epigenetic dysregulation can cause a loss of β cell identity, which is characterized by reduced expression of genes that are important for β cell function, ectopic expression of genes that are not supposed to be expressed in β cells, and loss of genetic imprinting. Consequently, this may lead to β cell dysfunction and impaired insulin secretion. Risk factors that can cause epigenetic dysregulation include parental obesity, an adverse intrauterine environment, hyperglycemia, lipotoxicity, aging, physical inactivity, and mitochondrial dysfunction. These risk factors can affect the epigenome at different time points throughout the lifetime of an individual and even before an individual is conceived. The plasticity of the epigenome enables it to change in response to environmental factors such as diet and exercise, and also makes the epigenome a good target for epigenetic drugs that may be used to enhance insulin secretion and potentially treat diabetes.
    Biochemistry and Cell Biology 08/2015; DOI:10.1139/bcb-2015-0057 · 2.15 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: journals.permissions@oup.com.
    Toxicological Sciences 02/2015; 143(2):231-41. DOI:10.1093/toxsci/kfu250 · 3.85 Impact Factor
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Nov 11, 2014