Epigenetics Lights Up the Obesity Field

Marti, Amelia; Ordovas, José M.

doi:10.1159/000329847

Cited by 16 publications

(10 citation statements)

References 27 publications

(39 reference statements)

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“…A list of additional resources on epigenomic research such as the human epigenome project initiative (www.epigenome.org) can be found in Marti and Ordovas. 19 The mechanism leading to loss of DNA methylation is still disputed. 20 The dynamic nature of DNA methylation is illustrated by the age-dependent progression of epigenetic changes suggested by larger differences in global DNA methylation patterns in older pairs than younger pairs of monozygotic twins.…”

Section: Methylation Of Dnamentioning

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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Section: Methylation Of Dnamentioning

confidence: 99%

Epigenetic regulation in obesity

2011

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Section: Introductionmentioning

confidence: 99%

“…Genome-wide association studies have identified more than 40 loci related to human obesity, and the fat mass and obesity-associated (FTO) gene is the most replicated and shows the highest statistical significance (Marti & Ordovas 2011). However, the combined effect of all of these loci only account for 2-3% of the inherited contribution to obesity risk (Marti & Ordovas 2011), which highlights the multifactorial and complex nature of the disease. It is therefore generally accepted that 'common obesity' is driven by the sensitivity of an individual's genetic predisposition to the harmful effects of environmental influences, such as increased energy intake (particularly of high-energy density (HED) diets) and sedentary lifestyle.…”

Section: Introductionmentioning

confidence: 99%

Contribution of the hypothalamus and gut to weight gain susceptibility and resistance in mice

Fam¹,

Sgambellone²,

Ruan³

et al. 2015

Journal of Endocrinology

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Obesity susceptibility in humans and in rodent strains varies in response to the consumption of high-energy density (HED) diets. However, the exact mechanism(s) involved in this susceptibility remain(s) unresolved. The aim of the present study was to gain greater insight into this susceptibility by using C57BL/6J (B6) mice that were separated into obesity-prone (diet-induced obese (DIO)) and obesity-resistant (diet-induced resistant (DR)) groups following an HED diet for 6 weeks. Physiological, biochemical and gene expression assessments of energy balance were performed in the DIO and DR mice on an HED diet and chow-fed mice. The increased weight gain of the DIO mice as compared to the DR mice was associated with increased energy intake and higher plasma leptin and adiponectin levels but not with reduced physical activity or resting energy expenditure. Hypothalamic Pomc gene expression was elevated, but there were no changes in Npy or Agrp expression. Adipose tissue leptin and adiponectin gene expression were significantly reduced in the DIO group as compared to the DR group. Interestingly, ileum expression of G protein-coupled receptor (Gpr) 40 (Gpr40) was significantly increased, whereas Gpr120, Gpr119, Gpr41, and glucagon-like peptide 1 (Glp1) were reduced. Contrastingly, the lower weight gain of the DR group was associated with elevated adipose tissue leptin and adiponectin gene expression, but there were no differences in plasma hormone or hypothalamic gene expression levels as compared to chow-fed mice. Therefore, the present data demonstrate that susceptibility and resistance to diet-induced weight gain in B6 mice appears to be predominantly driven by peripheral rather than hypothalamic modifications, and changes in gut-specific receptors are a potentially important contributor to this variation. Key Words" diet-induced obesity " high-energy density diet " body weight regulation

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“…Due to the high economic and social impact of obesity and its comorbidities [3,4], prevention is a priority, as is understanding the factors leading to obesity in younger ages. Although there is a genetic component in the susceptibility to obesity and related disorders, the final outcome will depend on the interaction of each individual's genetic background with their exposure to more or less obesogenic environments that encourage inadequate eating habits or sedentary behaviors [5,6].…”

Section: Tackling Obesity In Children and Adolescentsmentioning

confidence: 99%