Abstract
Nowadays, it is well-known that the deregulation of epigenetic machinery is a common biological event leading to the development and progression of metabolic disorders. Moreover, the expression level and actions of leptin, a vast adipocytokine regulating energy metabolism, appear to be strongly associated with epigenetics. Therefore, the aim of this review was to summarize the current knowledge of the epigenetic regulation of leptin as well as the leptin-induced epigenetic modifications in metabolic disorders and associated phenomena. The collected data indicated that the deregulation of leptin expression and secretion that occurs during the course of metabolic diseases is underlain by a variation in the level of promoter methylation, the occurrence of histone modifications, along with miRNA interference. Furthermore, leptin was proven to epigenetically regulate several miRNAs and affect the activity of the histone deacetylases. These epigenetic modifications were observed in obesity, gestational diabetes, metabolic syndrome and concerned various molecular processes like glucose metabolism, insulin sensitivity, liver fibrosis, obesity-related carcinogenesis, adipogenesis or fetal/early postnatal programming. Moreover, the circulating miRNA profiles were associated with the plasma leptin level in metabolic syndrome, and miRNAs were found to be involved in hypothalamic leptin sensitivity. In summary, the evidence suggests that leptin is both a target and a mediator of epigenetic changes that develop in numerous tissues during metabolic disorders.
Highlights
Metabolic syndrome (MetS) is a cluster of different pathological conditions that are extremely common among modern societies
Leptin is a hormone exhibiting an anorexic effect, whose discovery confirmed that adipose tissue (AT) is an endocrine organ involved in energy metabolism [5]
Well-known that any insult including stress, famine, gestational diabetes, excess pregnancy weight gain, While it is well-known that any insult including stress, famine, gestational diabetes, excess pregnancy or even high-fructose diet may have a sustained impact on the intrauterine milieu and the development weight gain, or even high-fructose diet may have a sustained impact on the intrauterine milieu and of the fetus, it appears that even paternal obesity plays a role [109,110,111]
Summary
Metabolic syndrome (MetS) is a cluster of different pathological conditions that are extremely common among modern societies. Hypertrophy of visceral adipose tissue (VAT), but not subcutaneous adipose tissue (SAT), is an independent risk factor for the most common obesity-associated disorder, type 2 diabetes (T2DM). Adipocytokines are bioactive peptides produced by adipose depots that play an essential role in the regulation of insulin signaling, glucose transport, lipid metabolism, and inflammation [4]. Leptin is a hormone exhibiting an anorexic effect, whose discovery confirmed that adipose tissue (AT) is an endocrine organ involved in energy metabolism [5]. T2DM, and MetS have been found to be associated with deregulated serum leptin levels, while leptin resistance has been recognized as an important factor in obesity [6,7,8,9]. In this review, we focused on recent achievements in the field of the epigenetic regulation of leptin as well as leptin-induced epigenetic phenomena in metabolic disorders such as the adipogenesis, fetal, and early postnatal programming of metabolism
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