Role of Epigenetic Modifications in Metabolic Diseases

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (17 September 2021) | Viewed by 4078

Special Issue Editor


E-Mail Website1 Website2
Guest Editor
1. Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, New York, NY 10065, USA
2. Department of Genetic Medicine, Weill Cornell Medicine-Qatar, Doha, Qatar
Interests: cardiovascular disease; diabetes; cardiology; DNA methylation; epigenetics

Special Issue Information

Dear Colleagues,

Epigenetics refers to the study of changes in gene activity regulation and expression that are not dependent on the DNA sequence. Recent evidence suggests that environmental factors, as well as traditional cardiovascular risk factors, may trigger modifications within the epigenome, hence affecting the expression of oxidative and inflammatory genes, inducing metabolic changes. On the other hand, these epigenomic modifications may also serve as biomarkers for the risk of cardiovascular disease development and progression. We would like to invite you to contribute to this Special Issue of Genes, entitled “Role of Epigenetic Modifications in Metabolic Diseases”.

Dr. Charbel Abi Khalil
Guest Editor

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Keywords

  • epigenetics
  • DNA methylation
  • non-coding RNAs
  • cardiovascular disease
  • diabetes
  • obesity
  • cardiology
  • metabolic diseases

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Published Papers (1 paper)

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Research

12 pages, 1617 KiB  
Article
PPARG Hypermethylation as the First Epigenetic Modification in Newly Onset Insulin Resistance in Human Adipocytes
by Małgorzata Małodobra-Mazur, Aneta Cierzniak, Krzysztof Kaliszewski and Tadeusz Dobosz
Genes 2021, 12(6), 889; https://doi.org/10.3390/genes12060889 - 9 Jun 2021
Cited by 18 | Viewed by 3284
Abstract
Insulin acts by binding with a specific receptor called an insulin receptor (INSR), ending up with glucose transporter activation and glucose uptake. Insulin resistance (IR) is a state when the physiological amount of insulin is not sufficient to evoke proper action, i.e., glucose [...] Read more.
Insulin acts by binding with a specific receptor called an insulin receptor (INSR), ending up with glucose transporter activation and glucose uptake. Insulin resistance (IR) is a state when the physiological amount of insulin is not sufficient to evoke proper action, i.e., glucose uptake. Epigenetic modifications associated with obesity and IR are some of the main mechanisms leading to IR pathogenesis. The mesenchymal stem cells of adipose tissue (subcutaneous (SAT) and visceral (VAT)) were collected during abdominal surgery. IR was induced ex vivo by palmitic acid. DNA methylation was determined at a global and site-specific level. We found higher global DNA methylation in IR adipocytes after 72 h following IR induction. Furthermore, numerous genes regulating insulin action (PPARG, SLC2A4, ADIPOQ) were hypermethylated in IR adipocytes; the earliest changes in site-specific DNA methylation have been detected for PPARG. Epigenetic changes appear to be mediated through DNMT1. DNA methylation is an important component of IR pathogenesis; the PPARG and its epigenetic modification appear to be the very first epigenetic modification in newly onset IR and are probably of the greatest importance. Full article
(This article belongs to the Special Issue Role of Epigenetic Modifications in Metabolic Diseases)
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