Curr Pharm Des. 2017 Aug 22. doi: 10.2174/1381612823666170823101713.
Blum K1, Thanos PK2, Wang GJ3, Febo M1, Demetrovics Z4, Modestino EJ5, Braverman ER6, Baron D6, Badgaiyan RD7, Gold MS8.
Abstract
Obesity is damaging the lives of more than 300 million people worldwide and maintaining a healthy weight using popular weight loss tactics remains a very difficult undertaking. Managing the obesity problem seems within reach, as better understanding develops, of the function of our genome in drug/nutrient responses. Strategies indicated by this understanding of nutriepigenomics and neurogenetics in the treatment and prevention of metabolic syndrome and obesity include moderation of mRNA expression by DNA methylation, and inhibition of histone deacetylation. Based on an individual’s genetic makeup deficient metabolic pathways can be targeted epigenetically by, for example, the provision of dietary supplementation that includes phytochemicals, vitamins, and importantly functional amino acids. Also, the chromatin structure of imprinted genes that control nutrients during fetal development can be modified. Pathways affecting dopamine signaling, molecular transport and nervous system development are implicated in these strategies. Obesity is a subtype of Reward Deficiency Syndrome (RDS) and these new strategies in the treatment and prevention of obesity target improved dopamine function. It is not merely a matter of gastrointestinal signaling linked to hypothalamic peptides, but alternatively, finding novel ways to improve ventral tegmental area (VTA) dopaminergic function and homeostasis.
KEYWORDS: Food and drug addiction; epigenetics. ; hypothalamic-gut-axis; neurogenetics; pro-dopamine regulation; reward deficiency syndrome (RDS)
PMID: 28831923
DOI: 10.2174/1381612823666170823101713
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