By Jim Kaput, Raymond L. Rodriguez
ISBN-10: 0471683191
ISBN-13: 9780471683193
The definitive advisor to the elemental ideas and most modern advances in dietary GenomicsThough nonetheless in its infancy, dietary genomics, or "nutrigenomics," has printed a lot concerning the complicated interactions among vitamin and genes. however it is in its strength functions that nutrigenomics provides to revolutionize the methods we deal with human health and wellbeing and wrestle sickness within the years forward. nice development already has been made in modeling "personalized" food for optimum well-being and sturdiness in addition to in genotype-based nutritional interventions for the prevention, mitigation, or attainable remedy of a number of power illnesses and a few varieties of cancer.Topics coated include:* nutrition and gene expression* The position of metabolomics in individualized wellbeing and fitness* Molecular mechanisms of toughness legislation and calorie restrict* eco-friendly tea polyphenols and soy peptides in melanoma prevention* Maternal nutrients and fetal gene expression* Genetic susceptibility to heterocyclic amines from cooked meals* Bioinformatics and biocomputation in nutrigenomics* The pursuit of optimum dietsWritten through an all-star crew of specialists from world wide, this quantity presents an built-in evaluation of the state-of-the-art box of dietary genomics. The authors and editors lead an in-depth dialogue of the basic ideas and clinical methodologies that function the root for dietary genomics and discover very important contemporary advances in an array of similar disciplines. every one self-contained bankruptcy builds upon its predecessor, best the reader seamlessly from uncomplicated rules to extra complicated medical findings and experimental designs. clinical chapters are rigorously balanced with these addressing the social, moral, regulatory, and advertisement implications of nutrigenomics.
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Additional resources for Nutritional Genomics: Discovering the Path to Personalized Nutrition
Example text
This genotype produces the A phenotype when these individuals eat a diet containing 32% fat, but a B phenotype when fed 10% fat—a result that can be explained by genotype–environment interactions. Chapter 13 in this volume provides a more detailed description of recent advances in this field. Although much attention in the nutrigenomics community is focused on gene regulation by dietary factors (Chapters 7, 11, and 14 in this volume), dietary chemicals also alter the activity of proteins and enzymes directly.
The incidence or severity of subphenotypes of the disease is measured in F2 mice and statistically associated with chromosomal regions from each of the original parental strains. A given pair of inbred mice may have 10–15 regions that contribute to the complex phenotype in those strains. , [32]) because inbreeding selects for a subset of genetic variation. If one or more of the genes within the QTLs regions were mutated, each parental strain would develop the particular disease. This does not occur.
1. 0) have also been identified [16]. Some of these T2DM QTLs may be population specific, which can be explained by evolutionary history (see above), by differences in defining phenotypes or subphenotypes in each study, and by methodological differences. Developing standard data elements is a critical need for the development of nutrigenomic research (see Chapters 3 and 16 in this volume). 1. Type 2 diabetes mellitus (T2DM) quantitative trait loci (QTLs) for humans. See text. 3. Hypothetical Genotypes of Six Individuals at Seven Disease Locia QTL A B C D E F 1 2 3 4 5 6 7 + + + + + + + + o + + + + + o + + - o + + + o + - - Each individual inherits one of three alleles of each of the seven genes at QTLs 1 through 7.
Nutritional Genomics: Discovering the Path to Personalized Nutrition by Jim Kaput, Raymond L. Rodriguez
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