Research Topic

Epigenetic Control of Adaptive Thermogenesis

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The prevalence of metabolic disorders such as obesity and type 2 diabetes is rapidly growing throughout the globe because of the increased consumption of calorie-dense foods and sedentary lifestyle. Consequently, efficacious obesity therapies are needed to combat this epidemic. Recently, promoting energy ...

The prevalence of metabolic disorders such as obesity and type 2 diabetes is rapidly growing throughout the globe because of the increased consumption of calorie-dense foods and sedentary lifestyle. Consequently, efficacious obesity therapies are needed to combat this epidemic. Recently, promoting energy expenditure through enhancing adaptive thermogenesis has attracted much attention as a promising therapeutic approach for the treatment and prevention of obesity. Adaptive thermogenesis refers to the process of heat generation in response to the drop of environmental temperature and/or food intake. It includes shivering thermogenesis, non-shivering thermogenesis and diet-induced thermogenesis. Current studies are mostly focused on the non-shivering thermogenesis that occurs primarily in brown fat, partially in beige fat, and in skeletal muscle.

Thermogenesis at the cellular level requires the function of uncoupling proteins, which are capable of dissipating the proton gradient across the mitochondrial inner membrane while uncoupling it from the process of ATP production, but instead, for heat generation. In mammals, two types of fat cells are involved in the process of non-shivering thermogenesis: (1) classic brown adipocytes, which are derived from a myf-5 positive muscle-like cellular lineage, are the main components of brown fat and the major players in heat generation; (2) "brown-like" adipocytes residing within white adipose depots that are also referred to as "beige" or "brite" adipocytes. A common feature of both types of thermogenic fat cells is that they contain high density of mitochondria and selectively express high levels of the thermogenic marker gene uncoupling protein 1 (UCP1). Animal studies have clearly shown that the thermogenic activity of brown fat has a positive effect on maintaning whole body metabolic homeostasis. The ablation of brown fat or UCP1 knock-out leads to reduced energy expenditure and the onset of obese phenotype. The molecular aspects controlling/affecting thermogenic adipocyte development and function have been studied extensively, and among them, the epigenetic mechanisms were found to have significant effects. Epigenetic mechanisms include post-translational modifications (PTMs) on histones, DNA methylation, non-coding RNAs (miRNAs and long non-coding RNAs) and, more broadly, PTMs on non-histone regulators. In the last decade, numerous lines of evidence have emerged supporting the fundamental involvement of epigenetic modifications during adaptive thermogenesis.

In this Research Topic, we welcome contributions in the form of original research articles, reviews, and perspectives providing new insights into the epigenetic regulation of adaptive thermogenesis, in-depth analysis and discussion of the current available experimental results in this field, or the outlook for future directions.

The following specific themes will be addressed:

(1) Epigenetic regulation of gene expression network in adaptive thermogenesis;
(2) Epigenetic regulation of the functional activity of transcription factors and metabolic enzymes in adaptive thermogenesis; and
(3) Epigenetic mechanisms involved in the onset and progression of metabolic diseases through the regulation of adaptive thermogenesis.


Keywords: Epigenetics, Chromatin modification, Non-coding RNA, Adaptive thermogenesis, Metabolic diseases


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