Nutrigenomic Effects Research Articles

Grape‐Enriched Diets Alter Cardiac Pathology and Cardiac Glutathione Dynamics in Hypertensive Rats

Increased fruit and vegetable intake can reduce hypertension, but its effect upon hypertensive cardiac pathology is unknown. This relationship was tested in the Dahl‐Salt Sensitive rat fed a high‐salt diet. Provision of 3% (w:w) whole table grape powder for 18 weeks reduced blood pressure, reduced cardiac hypertrophy, improved cardiac function, and increased cardiac glutathione, a key endogenous antioxidant. Provision of vasodilator hydralazine matched the blood pressure reduction of grape but failed to similarly reduce cardiac pathology. In vitro, phytochemicals found in grapes can alter genes related to Phase I/II metabolism, impacting glutathione dynamics. However, cardiac effects with a whole food are unknown. RT‐PCR analysis indicated that grape provision altered genes for oxidoreductases, transferases, sulfotransferases and peroxidases which affect glutathione dynamics, which on balance, would favor elevated glutathione. Key expression changes are confirmed by immunoblot. Importantly, these changes were conserved in grape‐fed, healthy (low‐salt fed) rats, further supporting the nutrigenomic effects of grape intake. In conclusion, physiologically relevant phytochemical intake reduced hypertensive cardiac pathology and altered cardiac transcripts related to glutathione dynamics, which may be vital to its cardioprotective effects. California Table Grape Commission, NIH‐NHLBI.Grant Funding SourceNIH‐NHLBI, California Table Grape Commission

Incorporating Basic Nutrition Science into Health Interventions for Cancer Prevention

Increasing evidence points to numerous dietary components that modify cancer incidence as well as the biological behavior of tumors. These inhibitory or stimulatory effects depend not only on the dietary component examined, but on a number of factors including the cellular DNA profile (nutrigenetic and nutrigenomic effects), protein formation and regulation (proteomic effect), and the effective delivery of the active intermediate at specific target sites (metabolomic effect). Unfortunately, the diet and cancer research domain is strewn with studies that were inadequately designed to monitor biological endpoints, used invalid biomarkers, or monitored irrelevant intakes or exposures. The scientific frontiers in health risk prediction and disease prevention strategies will greatly expand with the building of reliable nutrition and cancer biomarker databases that use modeling techniques to integrate information about intakes, effect biomarkers, and susceptibility biomarkers. Fundamental to this database will be the elucidation of the specific molecular sites of action (targets) for the specific dietary component. Clustering techniques that build on either genes or ratios of genetic expressions or their products will be needed to assess the merit of a particular dietary intervention. Models are already surfacing about how dietary-induced fluctuations in genes and their expression products can modify pathways associated with carcinogen activation and detoxification, alter rates of cellular proliferation, influence apoptosis, and modify angiogenesis. Embracing new genomic technologies offers exciting opportunities for advancing nutrition, especially those related to cancer prevention. We must effectively communicate, within a responsible bioethical framework, the potential value of knowledge about genes and gene products.