“Nutritional genomics”的意思、由来-开放百科全书

Nutritional science originally emerged as a field that studied individuals lacking certain nutrients and the subsequent effects,^[1] such as the disease scurvy which results from a lack of vitamin C. As other diseases closely related to diet (but not deficiency), such as obesity, became more prevalent, nutritional science expanded to cover these topics as well.^[1] Nutritional research typically focuses on preventative measure, trying to identify what nutrients or foods will raise or lower risks of diseases and damage to the human body.

For example, Prader–Willi syndrome, a disease whose most distinguishing factor is insatiable appetite, has been specifically linked to an epigenetic pattern in which the paternal copy in the chromosomal region is erroneously deleted, and the maternal loci is inactivated by over methylation.^[3] Yet, although certain disorders may be linked to certain single-nucleotide polymorphisms (SNPs) or other localized patterns, variation within a population may yield many more polymorphisms.^[4]

Applications

Obesity is one of the most widely studied topics in nutritional genomics. Due to genetic variations among individuals, each person could respond to diet differently. By exploring the interaction between dietary pattern and genetic factors, the field aims to suggest dietary changes that could prevent or reduce obesity.^[5]

There appear to be some SNPs that make it more likely that a person will gain weight from a high fat diet; for people with AA genotype in the FTO gene showed a higher BMI compared those with TT genotype when having high fat or low carbohydrate dietary intake.^[5] The APO B SNP rs512535 is another diet-related variation; the A/G heterozygous genotype was found to have association with obesity (in terms of BMI and waist circumference) and for individuals with habitual high fat diet (>35% of energy intake), while individuals with GG homozygotes genotype are likely to have a higher BMI compared to AA allele carriers. However, this difference is not found in low fat consuming group (<35% of energy intake).^[5]

See also

References

1. ^¹²{{cite journal | last1 = Neeha | first1 = V. S. | last2 = Kinth | first2 = P. | year = 2013 | title = Nutrigenomics research: a review | url = | journal = Journal of Food Science and Technology | volume = 50 | issue = 3| pages = 415–428 | doi=10.1007/s13197-012-0775-z| pmc = 3602567 }}
2. ^{{cite journal|last1=Fenech|first1=Michael|last2=El-Sohemy|first2=Ahmed|last3=Cahill|first3=Leah|last4=Ferguson|first4=Lynnette R.|last5=French|first5=Tapaeru-Ariki C.|last6=Tai|first6=E. Shyong|last7=Milner|first7=John|last8=Koh|first8=Woon-Puay|last9=Xie|first9=Lin|last10=Zucker|first10=Michelle|last11=Buckley|first11=Michael|last12=Cosgrove|first12=Leah|last13=Lockett|first13=Trevor|last14=Fung|first14=Kim Y.C.|last15=Head|first15=Richard|title=Nutrigenetics and Nutrigenomics: Viewpoints on the Current Status and Applications in Nutrition Research and Practice|journal=Journal of Nutrigenetics and Nutrigenomics|volume=4|issue=2|year=2011|pages=69–89|issn=1661-6758|doi=10.1159/000327772|pmc=3121546}}
3. ^{{cite journal | pmc = 3717174|doi= 10.1111/nyas.12020 | pmid=23360386 | volume=1281 | title=The genetics of human obesity | year=2013 | journal=Ann N Y Acad Sci | pages=178–90 | last1 = Xia | first1 = Q | last2 = Grant | first2 = SF}}
4. ^Bisen, Prakash A.; Debnath, Mousumi; Prasad, Godavarthi B.K.S. (2010). Molecular Dianostics: Promises and Possibilities. Springer Science & Business Media. p. 26.{{ISBN|9048132614}}.
5. ^¹²{{Cite journal|title = Obesity: interactions of genome and nutrients intake|journal = Preventive Nutrition and Food Science|date = 2015-03-01|issn = 2287-1098|pmc = 4391534|pmid = 25866743|pages = 1–7|volume = 20|issue = 1|doi = 10.3746/pnf.2015.20.1.1|first = Miae|last = Doo|first2 = Yangha|last2 = Kim}}

Background and preventive health

Applications

See also

References