By Nilanjana Maulik, Gautam Maulik
As nutrients study is transferring its concentration from epidemiology and body structure to results of meals on the molecular point, a uniquely adapted nutrition that corresponds to the calls for of our genetic signature is rising as an quintessential want. utilizing high-throughput genomic instruments, nutrigenomics unravels the effect of micro- and macronutrients as powerful nutritional indications regulating metabolic pathways and unmasks how vulnerable genotypes are predisposed to diet-related illnesses.
Selected themes from this box were coated in a few books, yet no different finished textual content on epigenetics, meals, and human overall healthiness and disorder is out there, previously. This publication illustrates nutrition’s impact on epigenetic inheritance and the mechanisms underlying the amendment of the metabolic imprint of a person. This enriched realizing of nutrigenomics might be utilized to grasp a adapted nutrition which could alleviate imprinted metabolic syndromes. in particular, the booklet makes a speciality of:
<UL> * Maternal, perinatal, and neonatal nutrition
* Epigenetic mechanisms and cancer
* affects of nutritional components, folate deficiency and DNA methylation
* Nutrition’s impression on genetic imprinting
* the fundamentals of nutrigenomics and epigenetic regulation
Read or Download Nutrition, Epigenetic Mechanisms, and Human Disease PDF
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Additional resources for Nutrition, Epigenetic Mechanisms, and Human Disease
Mediterranean diet and survival among patients with coronary heart disease in Greece. Arch Int Med 165 (8):929. , P. Orfanos, and T. Norat. 2005. Modified Mediterranean diet and survival: EPIC-elderly prospective cohort study. Brit Med J 330 (7498):991. , Y. Chen, N. Zhu, C. Ho, Z. Zhou, and R. Rosen. 2000. Isolation and identification of stilbenes in two varieties of Polygonum cuspidatum. J Agric Food Chem 48(2):253–56. , S. Dessain, E. Eaton, S. Imai, R. Frye, T. Pandita, L. Guarente, and R. Weinberg.
CpG sites have been shown to act as hot spots for germline mutations, contributing to 30% of all point mutations in the germline, and for acquired somatic mutations that lead to cancer (Robertson and Wolffe 2000). For example, methylated CpG sites in the p53 tumor suppressor coding region contribute to as many as 50% of all inactivating mutations in colorectal cancer and to 25% of cancers in general (Robertson and Wolffe 2000). Increased DNMT1, 3a, and 3b and decreased MBD2 expression and activity have been observed in many human cancers (Li and Jaenisch 2000).
2005. Modified Mediterranean diet and survival: EPIC-elderly prospective cohort study. Brit Med J 330 (7498):991. , Y. Chen, N. Zhu, C. Ho, Z. Zhou, and R. Rosen. 2000. Isolation and identification of stilbenes in two varieties of Polygonum cuspidatum. J Agric Food Chem 48(2):253–56. , S. Dessain, E. Eaton, S. Imai, R. Frye, T. Pandita, L. Guarente, and R. Weinberg. 2001. hSIR2SIRT1 functions as an NAD-dependent p53 deacetylase. Cell 107 (2):149–59. , M. Mann and M. Bartolomei 2003. Genomic imprinting: intricacies of epigenetic regulation in clusters.