Epigenetics and Obesity

Campión, Javier; Milagro, Fermı́n I.; Martínéz, J. Alfredo

doi:10.1016/b978-0-12-375003-7.00011-x

Cited by 83 publications

(71 citation statements)

References 296 publications

(290 reference statements)

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“…However, epigenetics is emerging as a new framework for researching etiological factors and gene expression regulation in environment-related disease [10,12]. Indeed, epigenetics is the study of the changes in gene expression that are not directly due to variations in the DNA nucleotide sequence and can potentially be transmitted to the offspring [17].…”

Section: Introductionmentioning

confidence: 99%

Leptin and TNF-alpha promoter methylation levels measured by MSP could predict the response to a low-calorie diet

et al. 2011

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Obesity-associated adipose tissue enlargement is characterized by an enhanced proinflammatory status and an elevated secretion of adipokines such as leptin and cytokines such as TNF-alpha. Among the different mechanisms that could underlie the interindividual differences in obesity, epigenetic regulation of gene expression has emerged as a potentially important determinant. Therefore, twenty-seven obese women (age: 32-50 years; baseline Body Mass Index, BMI: 34.4±4.2 Kg/m 2 ) were prescribed an eightweek Low-Calorie-Diet and epigenetic marks were assessed. Baseline and endpoint anthropometric parameters were measured and blood samples were drawn. Genomic DNA and RNA from adipose tissue biopsies were isolated before and after the dietary intervention. Leptin and TNF-alpha promoter methylation were measured by MSP after bisulfite treatment and gene expression was also analyzed.Obese women with a successful weight loss (≥5% of initial body weight, n=21) improved the lipid profile and fat mass percentage (-12%, p<0.05). Both systolic (-5%, p<0.05) and diastolic (-8%, p<0.01) blood pressures significantly decreased. At baseline women with better response to the dietary intervention showed lower promoter methylation levels of leptin (-47%, p<0.05) and TNF-alpha (-39%, p=0.071) than the non-responder group (n=6), while no differences were found between responder and non-responder group in leptin and TNF-alpha gene expression analysis. These data suggest that leptin and TNF-alpha methylation levels could be used as epigenetic biomarkers concerning the response to a Low-CalorieDiet. Indeed, methylation profile could help to predict the susceptibility to weight loss as well as some comorbidities such as hypertension or type 2 diabetes.

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Section: Introductionmentioning

confidence: 99%

Leptin and TNF-alpha promoter methylation levels measured by MSP could predict the response to a low-calorie diet

et al. 2011

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“…This may in part explain previous contradictory results on genetic association for this single-nucleotide polymorphism to obesity. 49 In addition, a list of genes with reported variation in DNA methylation in promoter CpG islands, most detected in cancer, but with a biological function related to adipogenesis, inflammation, fat metabolism and insulin signaling, are reported by Campió n et al 50 Importantly, CpGs outside CpG islands, in promoters and elsewhere, and cytosines in non-CpG sites, have also been found to have variation in DNA methylation associated to metabolism-related phenotype. In fact, methylation of cytosine in non-CpG sites of PPARg coactivator-1a has been associated to type 2 diabetes.…”

Section: Epigenetic Factors In Obesitymentioning

confidence: 99%

Epigenetic regulation in obesity

2011

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The availability to the DNA strand and the activity of the transcription machinery is crucial for the cell to use the information in the DNA. The epigenetic mechanisms DNA methylation, modification of histone tails, other chromatin-modifying processes and interference by small RNAs regulate the cell-type-specific DNA expression. Epigenetic marks can be more or less plastic perpetuating responses to various molecular signals and environmental stimuli, but in addition apparently stochastic epigenetic marks have been found. There is substantial evidence from animal and man demonstrating that both transient and more long-term epigenetic mechanisms have a role in the regulation of the molecular events governing adipogenesis and glucose homeostasis. Intrauterine exposure such as poor maternal nutrition has consistently been demonstrated to contribute to a particular epigenotype and thereby developmental metabolic priming of the exposed offspring in animal and man. Epigenetic modifications can be passed not only from one cell generation to the next, but metabolic disease-related epigenotypes have been proposed to also be transmitted germ-line. Future more comprehensive knowledge on epigenetic regulation will complement genome sequence data for the understanding of the complex etiology of obesity and related disorder.

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“…In this context, epigenetic studies are contributing to unravel some putatively hidden phenomena that are not being explained by the accomplishment of the Human Genome Project in relation to obesity (55) . In the last few years, different examples of dynamic changes in DNA methylation patterns, histone covalent modifications and the involvement of non-coding RNA due to the restriction or supplementation with different nutrients have been reported (4,25,56) , but also in relation to obesity (57) . Thus, the methylation pattern of the leptin promoter in adipocytes is affected by a high fat intake in rats following an inverse trend to body weight changes (58) , while weight gain induced by an isoenergetic pair-fed high-fat diet produces a nutriepigenetic outcome on fatty acid synthase and NADH dehydrogenase ubiquinone 1b subcomplex subunit 6 gene promoters (59) .…”

Section: Animal Models and Epigenetic Regulationmentioning

confidence: 99%

“…Indeed, maternal nutrition can programme gene expression patterns to the embryo that persist into adulthood and may contribute to the appearance of typical metabolic syndrome features such as hypertension, insulin resistance, hyperlipaemia and abdominal obesity (24) . The parental conditions and lifestyles, which may involve maternal size/obesity, famine at perinatal periods, the use of nutritional supplements, alcohol or drug abuse as well as the administration of therapeutical agents in this critical period may alter specific processes with an impact on embryonic, placental and fetal growth, organogenesis or regulatory set points for system functions affecting adiposity, where inflammatory and immunologically mediated processes may be involved (25) . Interestingly, some of these epigenetically mediated signals may be not permanent but transient, which is of interest not only for prevention, but also as a target for developing future therapeutic focus (26) .…”

Section: The Developmental Origins Of Health and Disease Hypothesis Amentioning

confidence: 99%

“…One of the challenges in the epigenomics field is identifying and characterising the epigenetic marks and those stimuli modulating the expression of some specific genes (epiobesogenes) in pathways involving obesity/body weight homoeostasis and energy balance processes such as adipogenesis, inflammation, appetite, insulin signalling, thermogenesis or macronutrient turnover (25) . Indeed, a bioinformatics analysis of promoter regions for the search of epigenetic biomarkers of obesity, has identified putative methylation-prone sequence patterns in several obesityrelated genes such as fibroblast growth factor 2, phosphatase and tensin homolog deleted on chromosome 10, cyclin-dependent kinase inhibitor 1A and oestrogen receptor 1, implicated in adipogenesis, suppressor of cytokine signalling 1/suppressor of cytokine signalling 3, in inflammation and cytochrome c oxidase 7A1 lipoprotein lipase, caveolin 1 and insulin-like growth factor binding protein 3, in intermediate metabolism and insulin signalling (74) .…”

Section: Obesity Inflammation and Epigeneticsmentioning

confidence: 99%

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Interplay of early-life nutritional programming on obesity, inflammation and epigenetic outcomes

et al. 2012

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The huge health burden accompanying obesity is not only attributable to inadequate dietary and sedentary lifestyle habits, since a predisposing genetic make-up and other putative determinants concerning easier weight gain and fat deposition have been reported. Thus, several investigations aiming to understand energy metabolism and body composition maintenance have been performed considering the participation of perinatal nutritional programming and epigenetic processes as well as inflammation phenomena. The Developmental Origins of Health and Disease hypothesis and inheritance-oriented investigations concerning gene-nutrient interactions on energy homoeostasis and metabolic functions have suggested that inflammation could be not only a comorbidity of obesity but also a cause. There are several examples about the role of nutritional interventions in pregnancy and lactation, such as energetic deprivation, protein restriction and excess fat, which determine a cluster of disorders affecting energy efficiency in the offspring as well as different metabolic pathways, which are mediated by epigenetics encompassing the chromatin information encrypted by DNA methylation patterns, histone covalent modifications and non-coding RNA or microRNA. Epigenetic mechanisms may be boosted or impaired by dietary and environmental factors in the mother, intergenerationally or transiently transmitted, and could be involved in the obesity and inflammation susceptibility in the offspring. The aims currently pursued are the early identification of epigenetic biomarkers concerned in individual's disease susceptibility and the description of protocols for tailored dietary treatments/advice to counterbalance adverse epigenomic events. These approaches will allow diagnosis and prognosis implementation and facilitate therapeutic strategies in a personalised 'epigenomically modelled' manner to combat obesity and inflammation.

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Epigenetics and Obesity

Cited by 83 publications

References 296 publications

Leptin and TNF-alpha promoter methylation levels measured by MSP could predict the response to a low-calorie diet

Leptin and TNF-alpha promoter methylation levels measured by MSP could predict the response to a low-calorie diet

Epigenetic regulation in obesity

Interplay of early-life nutritional programming on obesity, inflammation and epigenetic outcomes

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