DNA methylation markers in obesity, metabolic syndrome, and weight loss

Samblas, Mirian; Milagro, Fermı́n I.; Martı́nez, Alfredo

doi:10.1080/15592294.2019.1595297

Cited by 173 publications

(151 citation statements)

References 167 publications

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“…It has been proven to be sensitive to external contributors, including food nutrition in mammals (22). Different food components and dietary nutrients are associated with DNA methylation that might contribute to obesity and other metabolic disorders in mammals (23). Palmitic acid increased the global DNA methylation levels of human pancreatic islets, FIGURE 2 | Scatterplot of the enriched top 20 Kyoto Encyclopedia of Genes and Genome pathways of differentially methylated genes (DMGs) that differentially methylated in the promoter (A) and the gene body regions (B).…”

Section: Discussionmentioning

confidence: 99%

“…It has been proven to be sensitive to external contributors, including food nutrition in mammals ( 22 ). Different food components and dietary nutrients are associated with DNA methylation that might contribute to obesity and other metabolic disorders in mammals ( 23 ). Palmitic acid increased the global DNA methylation levels of human pancreatic islets, reducing the secretion of insulin and raising the risk of T2D as a result ( 24 ).…”

Section: Discussionmentioning

confidence: 99%

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Changes of DNA Methylation Pattern in Metabolic Pathways Induced by High-Carbohydrate Diet Contribute to Hyperglycemia and Fat Deposition in Grass Carp (Ctenopharyngodon idellus)

et al. 2020

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Section: Discussionmentioning

confidence: 99%

“…It has been proven to be sensitive to external contributors, including food nutrition in mammals ( 22 ). Different food components and dietary nutrients are associated with DNA methylation that might contribute to obesity and other metabolic disorders in mammals ( 23 ). Palmitic acid increased the global DNA methylation levels of human pancreatic islets, reducing the secretion of insulin and raising the risk of T2D as a result ( 24 ).…”

Section: Discussionmentioning

confidence: 99%

Changes of DNA Methylation Pattern in Metabolic Pathways Induced by High-Carbohydrate Diet Contribute to Hyperglycemia and Fat Deposition in Grass Carp (Ctenopharyngodon idellus)

et al. 2020

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“…DNA methylation has been suggested as a mechanism that could explain inter-individual variability in terms of weight loss response as well as the metabolic response to weight loss (95). In this regard, there is interest in examining whether weight loss might reverse abnormal DNA methylation changes observed in obesity and thereby reduce comorbidities.…”

Section: Molecular Mechanisms Contributing To Obesity and Breast Cancmentioning

confidence: 99%

The Many Faces of Obesity and Its Influence on Breast Cancer Risk

2019

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Obesity is associated with increased risk of breast and other cancers. However, the complexity of the underlying mechanisms, together with the interplay of diet and physical activity-contributing to energy balance-and the role of adipose tissue, pose challenges to our understanding of the basis of this increased risk. Epidemiologic studies have documented a higher obesity prevalence in US black women compared to white women. Elucidation of the contribution of potential biological differences among racially distinct groups to their differences in breast cancer (BC) risk and mortality have been topics of considerable interest in recent years. The racial and ethnic variation in body fat distribution may account for at least part of the differences in breast cancer rates in these populations. Yet, while black women exhibit higher rates of obesity compared to white women, this does not translate directly into higher rates of BC. In fact, overall, BC in black women occurs with a lower incidence than BC in white women. Obesity is a known risk factor for postmenopausal breast cancer, and growing evidence suggests that abdominal obesity, also known as central obesity, may increase risk for triple negative breast cancer, which is more common in premenopausal women. The positive association of postmenopausal BC risk and specifically estrogen receptor (ER)-positive BC, is presumably due largely to accumulation of estrogen in the adipose tissue of the breast and other tissues. Of the two main types of adipose tissue-subcutaneous and visceral-visceral adipocytes are more active metabolically. Such adipose tissue harbors multiple molecular entities that promote carcinogenesis: endocrine molecules/hormones, immunologic factors, inflammatory cytokines, metabolic alterations, and other components of the microenvironment. Expression of these culpable entities is largely regulated by epigenetic mechanisms. The interrelationship between these entities and drivers of epigenetic alteration are critical to the regulation of pathways connecting obesity and cancer risk. Initiatives to counteract the carcinogenic effects of obesity have primarily involved modulation of energy balance by diet. However, targeting of specific molecular abnormalities characterizing adiposity offers an alternative approach to preventing cancer. Our goal in this review is to first discuss the major mechanisms contributing to the obesity-breast cancer link. We will also consider race, specifically black/white differences, as they relate to the association of obesity with breast cancer risk. Then we will enumerate strategies targeting these mechanisms to reduce BC risk, in large part by way of dietary interventions with potential to mitigate the cancer-promoting components of adiposity.

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“…High-fat feeding may also induce DNA methylation changes at key metabolic genes that could influence their expression and predisposing to metabolic dysfunctions [58].…”

Section: Nutritional Factors Affecting Dna Methylationmentioning

confidence: 99%

Nutritional Factors, DNA Methylation, and Risk of Type 2 Diabetes and Obesity: Perspectives and Challenges

Parrillo

Spinelli

Nicolò

et al. 2019

IJMS

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A healthy diet improves life expectancy and helps to prevent common chronic diseases such as type 2 diabetes (T2D) and obesity. The mechanisms driving these effects are not fully understood, but are likely to involve epigenetics. Epigenetic mechanisms control gene expression, maintaining the DNA sequence, and therefore the full genomic information inherited from our parents, unchanged. An interesting feature of epigenetic changes lies in their dynamic nature and reversibility. Accordingly, they are susceptible to correction through targeted interventions. Here we will review the evidence supporting a role for nutritional factors in mediating metabolic disease risk through DNA methylation changes. Special emphasis will be placed on the potential of using DNA methylation traits as biomarkers to predict risk of obesity and T2D as well as on their response to dietary and pharmacological (epi-drug) interventions.

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DNA methylation markers in obesity, metabolic syndrome, and weight loss

Cited by 173 publications

References 167 publications

Changes of DNA Methylation Pattern in Metabolic Pathways Induced by High-Carbohydrate Diet Contribute to Hyperglycemia and Fat Deposition in Grass Carp (Ctenopharyngodon idellus)

Changes of DNA Methylation Pattern in Metabolic Pathways Induced by High-Carbohydrate Diet Contribute to Hyperglycemia and Fat Deposition in Grass Carp (Ctenopharyngodon idellus)

The Many Faces of Obesity and Its Influence on Breast Cancer Risk

Nutritional Factors, DNA Methylation, and Risk of Type 2 Diabetes and Obesity: Perspectives and Challenges

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