Epigenetics and Metabolism in Health and Disease

Abstract

In the next 10 years, one billion people are estimated to suffer from disabling consequences of metabolic disorders, making them the number one noncommunicable disease on a global scale by 2030. Lots of risk factors such as dietary intake, lack of exercise and other life style behaviors are considered to play a role in the development of metabolic disorders. Despite the efforts that have been undertaken to unravel their potential causes, the underlying molecular mechanisms remain elusive. Evidence suggests that the pathogenesis involves changes on chromatin and chromatin-modifying enzymes, which can contribute to a persistent dysregulated metabolic phenotype. Indeed, a rising number of studies links epigenetic alterations with the diagnosis and prognosis of metabolic disorders. A prerequisite for exploiting these findings for pharmacological intervention is a detailed understanding of how differential epigenetic modifications control cell metabolism. In this mini review, we summarize the recent advances in uncovering the interplay between epigenetics and metabolic pathways on a cellular level and highlight potential new avenues for alternative treatment strategies.

Epigenome-wide analysis of common warts reveals aberrant promoter methylation

“…Moreover, atypical HF3B expression was reported to be associated with colorectal cancer and chondroblastoma [34,35]. On a similar note, epigenetic modifications have been linked to changes in metabolism in a number of different non-communicable diseases, including cancer and diabetes [36]. In the present study, promoters were differentially methylated within the 17β-hydroxysteroid dehydrogenase type 14 (HSD17B14), leukotriene C4 synthase (LTC4S), folate receptor 3 (FOLR3), alcohol dehydrogenase 7 (ADH7), and adiponectin receptor 2 (ADIPOR2) genes that are involved in steroid, eicosanoid, folate, retinol, and glucose and lipid metabolism, respectively [37][38][39][40][41].…”

Therapeutic Potentials of İnhibition Jumonji C Domain Containing Demethylases in Acute Myeloid Leukemia

“…If abnormal JmjC demethylase activity is modulated, it can lead to normal transcriptional arrangements. Therefore, JmjC domain inhibitors might have therapeutic potentials for the treatment of cancer [24,25,26,27].…”

The interaction between gut microbiome and nutrients on development of human disease through epigenetic mechanisms

“…Peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α; encoded by the PPARGC1A) serves as a transcriptional coactivator in mitochondria and has a function in oxidative metabolism. PRMT1 mediated cytosine methylation in PGC-1α which is expressed in brown adipose tissue involved in energy metabolism and diabetes [25].…”