Epigenetics of metabolic syndrome

Carson, Caryn; Lawson, Heather A.

doi:10.1152/physiolgenomics.00072.2018

Cited by 40 publications

(26 citation statements)

References 111 publications

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“…An accumulating amount of data suggests the strong interplay between all known components of epigenetic machinery, forming a so-called miRNA-epigenetic feedback loop to affect gene expression and take part in the development of various diseases [28]. Except for RNA methylation, all other types of epigenetic mechanisms have been demonstrated as deregulated in multiple tissues by inflammation, obesity, IR, T2DM, metabolic syndrome, gestational diabetes, or in the context of adipogenesis and fetal metabolic programming [29,30,31,32,33,34,35].…”

Section: Mechanisms Of Epigenetic Modificationsmentioning

confidence: 99%

Molecular Insight into the Interaction between Epigenetics and Leptin in Metabolic Disorders

et al. 2019

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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.

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Section: Mechanisms Of Epigenetic Modificationsmentioning

confidence: 99%

Molecular Insight into the Interaction between Epigenetics and Leptin in Metabolic Disorders

et al. 2019

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“…High maternal prepregnancy body mass index also led to altered DNA methylation levels in offspring [38]. This indicate the involvement of epigenetic mechanisms in the MetS development; and this issue is actively studied now [30,40].…”

Section: Epidemiology Causes and Complications Of Metsmentioning

confidence: 93%

Metabolic Syndrome, Obesity, and Drosophila

Bayliak

2020

jpnu

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Metabolic syndrome (MetS) is a cluster of metabolic disturbances increasing a risk of cardiovascular diseases and diabetes 2 types. The main features of MetS include atherogenic dyslipidemia, elevated blood pressure, insulin resistance and elevated glucose levels, a pro-thrombotic state, pro-oxidant and pro-inflammatory states. Excessive consumption of high caloric food and sedentary lifestyle followed by overweight and obesity, as well as aging and stresses are major contributing factors to the MetS development. MeS affects between 10 and 84% of adults depending on the used MetS criteria and increases significantly a risk of cardiovascular diseases, diabetes 2 type and kidney diseases. Patients with metabolic disorders like obesity, diabetes, cardiovascular, and liver disease may have a higher risk of infection of COVID-19 with significantly worse prognosis and outcomes in these patients. In recent years, the fruit fly, Drosophila melanogaster, has been actively used to study human metabolic disorders as a cost-effective and expedient model. Drosophila belongs to insects with full metamorphosis and its life cycle includes four developmental stages: embryo, larva, pupa, and adult flies. Each developmental stage has its own specific advantages and can be used to study metabolic homeostasis. Studies of metabolic disturbances in Drosophila and mammalian models along with humans have demonstrated that flies and small mammalian models have many similarities with humans in basic metabolic functions and share many molecular mechanisms which regulate these metabolic processes. In this paper, we describe the advantages and limitations of Drosophila models of metabolic syndrome and obesity in light of physiological and biochemical similarities and differences between insects and mammals.

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“…DNA methylation, histone modifications, and non-coding RNAs, such as microRNAs (miRNAs), are involved in epigenetic mechanisms that regulate gene expression and biological processes. miRNAs have been shown to modulate adipogenesis, insulin signaling, and other metabolic pathways, and their dysregulation was associated with obesity and MetS [ 10 , 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

Peripheral Blood miRome Identified miR-155 as Potential Biomarker of MetS and Cardiometabolic Risk in Obese Patients

Cerda

Amaral

Oliveira

et al. 2021

IJMS

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This study explored circulating miRNAs and target genes associated with metabolic syndrome (MetS) and cardiometabolic risk in obese patients. Small-RNA sequencing was used to assess the peripheral blood miRNome of 12 obese subjects (6 MetS and 6 non-MetS). Differentially expressed miRNAs and target genes were further analyzed by qPCR in a larger sample of obese patients (48 MetS and 32 non-MetS). miRNA:mRNA interactions were studied using in silico tools. miRNome analysis identified 10 downregulated miRNAs in MetS compared to non-Met patients (p < 0.05). In silico studies revealed three miRNAs (miR-155, miR-181a, and let-7a) and their predictive targets (CCAAT/enhancer-binding protein beta—CEBPB, KRAS proto-oncogene, GTPase—KRAS and suppressor of cytokine signaling 1—SOCS1) with a potential role in the insulin receptor signaling pathway. miR-155 expression was reduced and CEBPB mRNA levels were increased in MetS patients (p < 0.05), and these effects were correlated with the number of MetS diagnostic criteria (p < 0.05). Increased HOMA-IR (>7.6) was associated with low miR-155 levels, high CEBPB expression, and serum hsCRP (p < 0.05). miR-155 was negatively correlated with CEBPB, HOMA-IR, and plasma fibrinogen, and positively correlated with serum adiponectin (p < 0.05). Downregulation of circulating miR-155 is associated with insulin resistance, poor glycemic control, and increased MetS-related cardiometabolic risk, and these effects are potentially mediated by interaction with CEBPB.

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Epigenetics of metabolic syndrome

Cited by 40 publications

References 111 publications

Molecular Insight into the Interaction between Epigenetics and Leptin in Metabolic Disorders

Molecular Insight into the Interaction between Epigenetics and Leptin in Metabolic Disorders

Metabolic Syndrome, Obesity, and Drosophila

Peripheral Blood miRome Identified miR-155 as Potential Biomarker of MetS and Cardiometabolic Risk in Obese Patients

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