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The relationships between diet and health are becoming more and more substantial, in particular with respect to the most prominent chronic diseases. The maintenance of health and the prevention and treatment of chronic diseases are influenced by naturally occurring chemicals in foods. In addition to supplying the substrates for producing energy, a large number of dietary chemicals are bioactive; that is, they alter the regulation of biological processes and, either directly or indirectly, the expression of genetic information. Nutrients and bioactives may produce different physiological and phenotypes among individuals because of genetic variability and not only alter health, but also disease initiation, progression and severity.

The study and application of gene-nutrient interactions is called nutritional genomics or nutrigenomics. Nutrigenomics is the study of the effects of foods and food constituents on gene expression. It is about how our DNA is transcribed into mRNA and then to proteins and provides a basis for understanding the biological activity of food components. Nutrigenomics has also been described by the influence of genetic variation on nutrition by correlating gene expression or single-nucleotide polymorphisms with a nutrient`s absorption, metabolism, elimination or biological effects. By doing so, nutrigenomic aims to develop rational means to optimize nutrition, with respect to the subject`s genotype. Many kind of protein are made according to the sequence of mRNA, and they play many important roles in maintenance of cell structure, metabolism, signal transduction, defense response and various scenes in living organisms. When the functional ingredients or whole foods are applied, it will affect on the profile of gene expression in cells directly or indirectly. These change in gene expression result in the various physiological effects and reflect the function of the foods. Thus, we can find and evaluate the function of food components or whole food by knowing the types and function of the gene whose expression level has fluctuated by them.

One paper that I have found in scientific journal reported the molecular basis of dietary obesity. The journal title is: DNA Microarray Analysis of Genes Differentially Expressed in Diet-Induced (Cafetaria) Obese Rats. Obesity Research Vol. 11 No.2 February 2003. The authors examined adipose tissue genes differentially expressed in an obesity model using DNA microarray analysis. Increased food intake and decreased energy expenditure associated to modern lifestyles have contributed to the widely spread of obesity development. Several arrays have been conducted in genetically obese animals, providing valuable new molecular insights despite some limitations. In this report, author analysis the effect of long-term high-fat intake on the expression pattern of 4500 full-length genes. Gene expression profile of adipose tissue from obese rats (cafeteria diet) was compared with control animals to search for changes in gene expression in response to a hypercaloric fat-rich diet. Sample mal Wistar rats (5 week old) were housed in cages under controlled conditions of light (12 hours of light/12 hours of dark) and temperature (22 + 2 ^oC). All experimental procedures were performed according to National and Institutional Guidelines for Animal Care and Use at the University of Navarra. Rats (20) were assigned into two dietary groups for 65 days. The control group (n=10) was fed with a standard laboratory pelleted diet and free access to water (6% calories from fat), whereas the second group (cafetaria diet, n=10) was fed a fat-rich hypercaloric diet containing pate, chips, chocolate, bacon, biscuits, and chow in a proportion of 2:1:1:1:1:1 (65% calories of fat). Food was offered ad libitum and food intake and body weight were measured daily. After the experimental feeding period, animals were euthanized and epididymal white adipose tissue was immediately removed, frozen in liquid nitrogen, and stored at -80 ^oC. Serum glucose, proteins, cholesterol, glycerol, triglycerides, and free fatty acids were analyzed using an Autoanalyzer by routine procedures. Plasma insulin was assayed by radioimmunoassay using ¹²⁵I-labeled insulin, whereas leptin was determined by radioimmunoassay. Results shows that Cafetaria (obese) rats weighed 50% more and had 2.5-fold higher level of epididymal fat and elevated levels of circulating leptin. Adipose genes differentially expressed in obese and control rats were categorized into five factors, hormone receptor and signal transduction, redox and stress proteins, and cellular cytoskleteon. Interestingly, the expression levels of a number of genes involved in lipid metabolism such as glycelol-3-phosphate dehydrogenase, stearoyl coenzyme A desaturase, together with the transcription factors implicated in adipocyte differentiation (CAAT/enhancer binding protein-α and peroxisome proliferator-activated receptor-γ), were significantly increased in obese animals compared with control. The most up-regulated transcripts were the ob (49.2-fold change) and the fatty acid-binding protein genes (15.7-fold change). In contrast, genes related to redox and stress protein were generally down-regulated in obese animals compared with the control. The study showed that in diet-induced obesity, the expression levels of some important genes implicated in lipid metabolism were up-regulated, whereas those related to redox and stress protein were down-regulated in obese animals compared with control. This pattern of gene expression may occur in human obesity case after high-fat intake.