内容

目次

Contributors. Foreword. Preface. Acknowledgments. 1. AnIntroduction and Overview of Nutritional Genomics: Application to Type 2Diabetes and International Nutrigenomics (Jim Kaput). Introduction.Understanding T2DM: the current view of T2DM and treatment options.Understanding T2DM: begin before conception. Understanding T2DM: geneticcomplexity. Understanding T2DM: QTLs in humans. Understanding T2DM:from birth onward. Understanding T2DM: metabolomics. UnderstandingT2DM: environmental influences. Understanding T2DM: environment is morethan diet. Understanding T2DM: data acquisition and analyses.Bioinformatics and biocomputation. Converting science into practice.Research ethics and genetic privacy. Health disparities. Public andinternational policies. Conclusion. Acknowledgement. References.2. The Pursuit of Optimal Diets: A Progress Report (Walter C. Willett).2.1 Introduction. 2.2 Considerations in defining an optimal diet. 2.3Dietary fat and specific fatty acids. 2.4 Carbohydrates. 2.5 Protein.2.6 Vegetables and fruits. 2.7 Calcium and dairy products. 2.8 Saltand processed meats. 2.9 Alcohol. 2.10 Vitamin and mineral supplements.2.11 The potential impact of optimal diet and lifestyle changes. 2.12Summary. 2.13 Acknowledgement. 2.14 References. 3. Gene -Environment Interactions: Defining the Playfield (Jose M. Ordovas and DoloresCorella). 3.1 Genetic variability. 3.2 How to detect geneticvariability?. 3.3 What to analyze?. 3.4 Environmental factors. 3.5Gene-environment interactions: focus on diet. 3.6 Common genetic variantsand their interaction with dietary factors. 3.7 Gene X Microorganismsinteractions. 3.8 The microbiome (microbiota). 3.9 Bringing alltogether. 3.10 References. 4. Metabolomics: Bringing Nutrigenomics toPractice in Individualized Health Asssessment (J. Bruce German, Cora J.Dillard, S. Luke Hillyard, Matthew C. Lange, Jennifer T. Smilowitz, Robert E.Ward, and Angela M. Zivkovic). 4.1 Introduction. 4.2 Opportunities forfoods and health. 4.3 Tools of metabolomics. 4.4 The future ofmetabolomics. 4.5 Genomics. 4.6 Metabolome assembly and annotation.4.7 Bioinformatics: knowledge management from genomics and metabolomics tohealth assessment. 4.8 Summary. 4.9 References. 5. Genetic andmolecular buffering of phenotypes (John L. Hartman, IV). 5.1 Introduction.5.2 Examples of buffering. 5.3 Experimental concepts for geneticbuffering analysis. 5.4 Experimental platforms for global geneticinteraction analysis. 5.5 Acknowledgments. 5.6 References. 6. Gene -Gene Epistasis and Gene - Environment Interactions Influence Diabetes andObesity (Sally Chiu, Adam L. Diament, Janis S. Fisler, and Craig H. Warden).6.1 Gene - gene and gene - environment interactions. 6.2 Epistasis andgene - environment interactions in obesity and diabetes. 6.3 Animal modelsfor detecting gene interactions. 6.4 Gene - gene interaction in obesityand diabetes. 6.5 Dietary fat in obesity and diabetes. 6.6 Maternaleffects. 6.7 Future directions and conclusions. 6.8 References. 7.Nutrients and Gene Expression (Gertrud U. Schuster). 7.1 Introduction.7.2 SREBPs and ChREBP: transcription factors, influenced by dietary lipidsand glucose. 7.3 Superfamily of nuclear receptors. 7.4 Nuclearreceptors- -structure and function. 7.5 Nuclear receptors as metabolicsensor. 7.6 Vitamins. 7.7 Phytoesterogens - nutrients mimickingestrogens . 7.8 Polymorphisms. 7.9 Concluding remarks. 7.10Acknowledgement. 7.11 References. 8. Green Tea Polyphenols and CancerPrevention (Shangqin Guo and Gail Sonenshein). 8.1 Introduction. 8.2Green tea and cancer epidemiology. 8.3 Animal models. 8.4 Mechanisms ofgreen tea action: molecular signaling pathways and gene targets. 8.5Clinical studies and the promise of tea in combinatorial therapy. 8.6Future directions and concluding remarks. 8.7 Acknowledgements. 8.8References. 9. Molecular Mechanisms of Longevity Regulation and CalorieRestriction (Su - Ju Lin). 9.1 A conserved longevity factor, Sir2. 9.2Molecular mechanisms of calorie reduction. 9.3 Role of NAD/NADH ratio inaging and human diseases. 9.4 Possible CR mimetics - small molecules thatregulate Sir2 activity. 9.5 The molecular targets of Sir2 proteins inmammals. 9.6 A possibly conserved longevity pathway. 9.7 Applicationsto nutritional genomics. 9.8 References. 10. Maternal Nutrition:Nutrients and Control of Expression (Craig A. Cooney). 10.1 Methylmetabolism. 10.2 DNA methylation, epigenetics, and imprinting. 10.3Endogenous retroviruses and genome integrity. 10.4 Epigenetics andnutrition can greatly modulate genetic predispositions. 10.5 Yellow mousemodels of epigenetic regulation. 10.6 A variety of maternal effects areseen in mice. 10.7 Rat models of maternal effects leading to diabetes.10.8 Maternal effects on memory and aging. 10.9 Epigenetic effects infoxes. 10.10 Epigenetic effects related to reproduction in humans.10.11 Nutrients and compounds that may affect early development andepigenetics. 10.12 Conclusion. 10.13 Acknowledgements. 10.14References. 11. Nutrient - Gene Interactions Involving Soy Peptide andChemopreventive Genes in Prostate Epithelial Cells (Mark Jesus M. Magbanua,Kevin Dawson, Liping Huang, Wasyl Malyj, Jeff Gregg, Alfredo Galvez, andRaymond L. Rodriguez). 11.1 Introduction. 11.2 Lunasin structure andfunction. 11.3 Lunasin treatment of prostate cancer and gene expressionprofiling. 11.4 Lunasin - induced gene expression profiles. 11.5 Genesfor apoptosis. 11.6 Genes involved in suppression of cell proliferation.11.7 Mitotic checkpoint genes. 11.8 Genes involved in proteindegradation. 11.9 Connexin 43 gene for the gap junction protein. 11.10Target verification using RT - PCR. 11.11 Conclusion. 11.12Acknowledgements. 11.13 References. 12. Enzymes Lose Binding Affinity(increase Km) for Coenzymes and Substrates with Age: A Strategy forRemediation (Bruce N. Ames, Jung H. Suh, and Jiankang Liu). 12.1Introduction. 12.2 Remediation by high B vitamin intake of variant enzymeswith poor binding affinity (Km) for coenzymes. 12.3 Deformation ofproteins in mitochondria with aging. 12.4 Non - mitochondrial enzymes thatare deformed with age. 12.5 Conclusion. 12.6 References. 13. Dietaryand Genetic Effects on Atherogenic Dyslipidemia (Ronald M. Krauss, MD, andPatty W. Siri, PhD, MS). 13.1 LDL represent a heterogeneous population.13.2 LDL subclasses are influenced by genes and the environment. 13.3Summary. 13.4 References. 14. Genistein And Polythenols in the Study ofCancer Prevention: Chemistry, Biology, Statistics and Experimental Design(Stephen Barnes, David B. Allison, Grier P. Page, Mark Carpenter, Gary L.Gadbury, Sreelatha Meleth, Pamela Horn-Ross, Helen Kim, Coral A. Lamartinere,and Clinton J. Grubbs). 14.1 Introduction. 14.2 Diet and cancer.14.3 Chemistry of the polyphenols. 14.4 Uptake, distribution, metabolism,and excretion of the polyphenols. 14.5 Polyphenols and cancer prevention.14.6 Mechanisms of action of polyphenols. 14.7 Importance of timingexposure to polyphenols. 14.8 Assessing events leading to cancer-lowdimensional approaches. 14.9 Statistical consequences of high dimensionalapproaches. 14.10 High dimensional systems and the importance of the falsediscovery rate. 14.11 DNA microarray analysis-high dimensional researchinto gene expression. 14.12 Proteomics analysis-an even bigger challenge.14.13 Statistical problems with fold-change in DNA microarray andproteomics analyses. 14.14 Design in experiments involving DNA microarrayand proteomics analysis. 14.15 The design. 14.16 Role of the computerin high dimensional analysis. 14.17 Acknowledgements. 14.18 References.15. Susceptibility to Exposure to Heterocyclic Amines from Cooked Food:Role of UDP-glucuronosyltransferases (Michael A. Malfatti and James S.Felton). 15.1 Introduction. 15.2 Genetic susceptibility. 15.3UDP-glucuronosyltransferase. 15.4 UDP-glucuronosyltransferasebiochemistry. 15.5 UDP-glucuronosyltransferase gene structure. 15.6Substrate specificity and selectivity. 15.7 Tissue distribution ofUPD-glucuronosyltransferase. 15.8 Gene regulation. 15.9 Geneticvariation. 15.10 UDP-glucuronosyltransferase and cancer susceptibility.15.11 Heterocyclic amine carcinogens in food. 15.12 Carcinogenicity ofPhIP. 15.13 Metabolism of PhIP. 15.14 UDP - glucuronosyltransferase andPhIP risk susceptibility. 15.15 Summary. 15.16 Acknowledgements.15.17 References. 16. The Informatics and Bioinformatics Infrastructure ofa Nutrigenomics Biobank (Warren A. Kibbe). 16.1 Introduction. 16.2 Nextgeneration biobanks. 16.3 Intended audience for this chapter. 16.4Regulatory and policy environment. 16.5 HIPAA Health Insurance Portabilityand Accountability Act of 1996. 16.6 GMPs, GLPs and GCPs. 16.7 Fundingof biobanks. 16.8 Biobanking in clinical trials. 16.9 Datastandards/semantic interoperability. 16.10 Other Standards Bodies: CDISC.16.11 Informatics infrastructure. 16.12 System architecture. 16.13Separation of the clinical trial/patient identity management from thegenotype/phenotype repository. 16.14 Database architecture/ data modeling.16.15 Design practices. 16.16 Pulling it all together. 16.17References. 17. Biocomputation and the Analysis of Complex Datasets inNutritional Genomics (Kevin Dawson, Raymond L. Rodriguez, Wayne Chris Hawkes,and Wasyl Malyj). 17.1 Introduction. 17.2 Nutritional genomics is partof high - throughput biology. 17.3 Gene expression arrays. 17.4Proteomics and metabolomics data. 17.5 Sources of complexity innutritional genomics. 17.6 Data sets in nutritional genomics. 17.7 Thelevel of complexity in gene expression experiments. 17.8 Dimensionalityreduction methods. 17.9 Case study (microarray experiment of a dietary -intervention). 17.10 Summary. 17.11 Acknowledgement. 17.12References. 18. Cultural Humility: A Contribution to Health ProfessionalEducation in Nutrigenomics (Melanie Tervalon). 18.1 Introduction. 18.2Cultural Humility. 18.3 Summary. 18.4 Goals and objectives: curriculumcontent. 18.5 Goals and objectives: curriculum design. 18.6 Curriculumstructure and content: didactics, small groups and videotaping. 18.7 Theteaching staff. 18.8 Evaluation. 18.9 Summary. 18.10 References.19. Nutrients and Norms: Ethical Issues in Nutritional Genomics (DavidCastle, Cheryl Cline, Abdallah S. Daar, Charoula Tsamis, and Peter A.Singer). 19.1 Proactive ethics and nutritional genomics. 19.2 Claims ofhealth benefits arising from nutrigenomics. 19.3 Managing nutrigenomicinformation. 19.4 Methods for delivering nutrigenomic services. 19.5Nutrigenomic products. 19.6 Access to nutrigenomics. 19.7 Conclusion.19.8 References. Glossary. Index.