Abstract

Obesity has become a global epidemic that has a negative impact on population health and the economy of nations. Genetic predispositions have been demonstrated to have a substantial role in the unbalanced energy metabolism seen in obesity. However, these genetic variations cannot entirely explain the massive growth in obesity over the last few decades. Accumulating evidence suggests that modern lifestyle characteristics such as the intake of energy-dense foods, adopting sedentary behavior, or exposure to environmental factors such as industrial endocrine disruptors all contribute to the rising obesity epidemic. Recent advances in the study of DNA and its alterations have considerably increased our understanding of the function of epigenetics in regulating energy metabolism and expenditure in obesity and metabolic diseases. These epigenetic modifications influence how DNA is transcribed without altering its sequence. They are dynamic, reflecting the interplay between the body and its surroundings. Notably, these epigenetic changes are reversible, making them appealing targets for therapeutic and corrective interventions. In this review, I discuss how these epigenetic modifications contribute to the disordered energy metabolism in obesity and to what degree lifestyle and weight reduction strategies and pharmacological drugs can restore energy balance by restoring normal epigenetic profiles.

Highlights

  • Recent research has found that obese people are more likely to suffer significant repercussions from the overlapping COVID19 pandemic [3]

  • Multiple studies have linked sleep deprivation to alterations in the epigenome, notably genes that influence circadian rhythm and are known to affect several metabolic functions [101,102]. These findings suggest that sleep disturbances may trigger epigenetic changes that contribute to obesity and metabolic diseases

  • In addition to DNA methylation, bariatric surgery has been shown to induce modification in miRNAs and long non-coding RNAs (lncRNAs) that regulate the cell cycle, cell development, lipid metabolism, inflammatory response, insulin resistance, and endocrine function [137–139]. These findings suggest that weight loss is associated with the reversal of obesity epigenetic patterns and the acquisition of more favorable profiles associated with improved inflammatory, metabolic, and vascular function

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Summary

Introduction

Science has contributed to an almost three-decade increase in the average person’s lifespan. The rising obesity prevalence is considered an epidemic that threatens to reduce current and future generations’ life expectancy and quality of life [1]. This will pose a considerable challenge to future healthcare finances. Overweight people account for more than 1.9 billion (39%) of the adult population, with over 650 million (13%) obese This enormous increase in obesity rates over the last few decades cannot be explained entirely by genetics. Obesity is still avoidable by improved lifestyle and everyday decisions regarding nutrition, physical exercise, and other lifestyle variables These variables have been found to alter DNA transcription and, how genes are expressed. I will provide an overview of the intricate interplay between epigenetics and energy metabolism in the context of obesity development and management

The Role of Epigenetics in Obesity
DNA Methylation
Histone Modifications
Non-Coding RNAs
Epigenetic Effects of Environmental Factors and Lifestyle
Obesogenic Exposures
Dietary Factors
Physical Activity
Sleep Deprivation
Alcohol Intake
Weight Loss Interventions
Epigenetic Drugs
Findings
Conclusions and Future Perspectives
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