Abstract
The global prevalence of metabolic disorders, such as obesity, diabetes and fatty liver disease, is dramatically increasing. Both genetic and environmental factors are well-known contributors to the development of these diseases and therefore, the study of epigenetics can provide additional mechanistic insight. Dietary interventions, including caloric restriction, intermittent fasting or time-restricted feeding, have shown promising improvements in patients’ overall metabolic profiles (i.e., reduced body weight, improved glucose homeostasis), and an increasing number of studies have associated these beneficial effects with epigenetic alterations. In this article, we review epigenetic changes involved in both metabolic diseases and dietary interventions in primary metabolic tissues (i.e., adipose, liver, and pancreas) in hopes of elucidating potential biomarkers and therapeutic targets for disease prevention and treatment.
Highlights
The continuous rise in metabolic diseases, such as obesity, type 2 diabetes (T2D; Table 1) and non-alcoholic fatty liver disease (NAFLD), is one of the leading causes of patient morbidity and mortality worldwide (Saklayen, 2018) and cannot be solely explained by the contribution of genetic and environmental factors
Abrogation of Lsd1 (Ucp1-Cre; Lsd1flox/flox) (Sambeat et al, 2016) or Jhdm2a (Jhdm2a−/−) (Inagaki et al, 2009; Tateishi et al, 2009) in mice results in increased body weight, fat accumulation, and impaired glucose homeostasis, as well as “whitening” of brown adipose tissue (BAT) and dysregulated fatty acid metabolism. These results suggest an important role for these H3K9 histone methyltransferases (HMTs) and histone demethylases (HDMs) in obesity resistance
Sirtuin 1 (SIRT1) gene and protein expression is significantly reduced in adipose tissue of high-fat diet (HFD)-fed mice (Yoshizaki et al, 2009, 2010) as well as in chronically obese patients in which it negatively correlates with their body mass index (BMI) (Costa Cdos et al, 2010; Gillum et al, 2011; Perrini et al, 2020)
Summary
The continuous rise in metabolic diseases, such as obesity, type 2 diabetes (T2D; Table 1) and non-alcoholic fatty liver disease (NAFLD), is one of the leading causes of patient morbidity and mortality worldwide (Saklayen, 2018) and cannot be solely explained by the contribution of genetic and environmental factors. SIRT1 gene and protein expression is significantly reduced in adipose tissue of HFD-fed mice (Yoshizaki et al, 2009, 2010) as well as in chronically obese patients in which it negatively correlates with their body mass index (BMI) (Costa Cdos et al, 2010; Gillum et al, 2011; Perrini et al, 2020).
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