Term Paper: Nutrigenomics Is an Important Field

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[. . .] Screenings are available for both conditions and diets can be regulated to prevent these problems.

Consider now potential mechanisms of how chemicals and substances in nutrients can affect gene expression. Some chemicals in foods act as ligands for receptors in the nucleus. Fatty acids such as palmitic and linoleic acids and vitamins such as Vitamin A are known to bind nuclear receptors. These receptors that bind the Fatty acids regulate the genes involved in fat-metabolism. These receptors belong to a family of peroxisome proliferator-activated receptors (PPAR). When a ligand binds to a receptor it starts a cascade of events that extend beyond the nucleus and cytoplasm to across cells and tissues. Thus gene expression is affected. Various proportions of chemicals also affect metabolic pathways. These chemicals influence metabolism by affecting enzyme action. These enzymes are proteins, which are gene products. Each metabolic pathway affects other related and secondary pathways. This in turn affects other enzymes, which are products of other genes. For example, sterols are twenty-seven carbon atom compounds. They are steroids with one alcohol group. Sterol regulatory element binding proteins are activated by protease enzymatic action. Chemicals associated with nutrients might promote sterol metabolism. These are regulated by changed in glucose levels and polyunsaturated fatty acid levels. Similarly, the carbohydrate-responsive element binding protein is activated with increased levels of glucose in the system. (Kaput & Rodriguez, 2004)

Signal transduction is an important process in cancer studies. Certain growth factors catalyze signal transduction. Signal transduction in cancer is the signaling mechanism for apoptosis or cell death. A misdirected or absent signal might prevent apoptosis which eventually gives rise to tumors and cancer. There are two signaling pathways in cell metabolism that have been studied extensively. These are the MAPK (mitogen activated protein kinase) and the caspase-apoptotic pathways. There is enough evidence to suggest that chemicals containing certain organic functional groups and/or certain functional characteristics might help in preventing apoptosis.

The MAPK pathway involves signal transduction where a protein involved in a cascade sends a message from protein to protein by means of phosphorylation and subsequent dephosophorylation. Serine and Threonine are two amino acids that are involved in this signaling pathway that is initiated by another amino acid, praline. This cascade often proceeds from extra cellular stimulus to the nucleus of the cell that houses the DNA and relevant alleles. Certain chemicals help regulate and modulate the MAPK signaling pathways, this restoring normal cellular processes and maintaining the normal life of the cell. These compounds have been identified as polyphenol (-)-epigallocatechin-3-gallate (EGCG) commonly found in green tea, 2(3)-tert-butyl-4-hydroxyanisole (BHA) found in synthetic antioxidants and tert-butyl-hydroquinone (tBHQ) found in certain vegetables. Once activated, the MAPK or its constituent pathways can activate transcription factors. Once modulated, the consequences to cell function and metabolism are important. Depending on the doses of chemopreventive chemicals, the MAPK pathway induced by different activating factors can also be impeded. A polyphenolic compound isolated from grape seeds has been found to inhibit the growth of both breast and prostate cancer cells. These results are from studies that have been performed in vitro. (Hu & Kong, 2004)

Apoptosis is an important part of metabolism. This is because cells have to die once their function is complete so that new cells can take their place. The prevention of cell death is an important consideration because it essentially results in cells forming tumors. Receptors such as tumor necrosis factor receptor, Apo2 and Apo3 (among others) are responsible for inducing apoptosis. These receptors begin a signal transduction process. The signal is passed down until a group of proteins downstream in this pathway called capsases complete the apoptosis process. Apoptosis is regulated and controlled in the mitochondria. It is here that a balance is achieved between preventing both premature cell death and ensuring normal cell death. The role of various chemicals (in addition to environmental factors) that can induce apoptosis. (Hu & Kong, 2004)

Though heart disease is not reversible, the progress can be halted with lifestyle and dietary changes. In addition to blood pressure measurements, cholesterol measurements, specifically low-density lipoprotein cholesterol (LDL) and high-density lipoprotein cholesterol are good biomarkers when it comes to identifying tendency towards cardiovascular diseases.

LDL measurements are especially important. From a genetic standpoint however, there are more than one co-factor that contributes to CVD. They are lipid-binding proteins, apolipoproteins and certain enzymes are a few among many. Genetic variability has been identified in apolipoproteins among individuals. This is directly related to how the LDL changes with change in diets. Among other patients, abnormal lipid metabolism and lipoprotein profiles are indicators of atherosclerosis. (van Ommen & Stierum, 2002)

The question remains, what constituent chemicals have been identified as necessary in the maintenance of health. One might surmise that in order to study regulation of gene expression, one need to know what chemicals have to be studied. These chemicals have to be at an epidemiological level, found to have been beneficial in treating the symptoms of a disease or a disease itself. These chemicals have been identified as micronutrients, because they are required in small amounts in metabolic activities. If one identifies their role in regulating specific gene expression, then one can view these micronutrients as catalysts. Vitamin sB and E, and carotenoids have been identified as being beneficial in cardiovascular diseases. More specifically, vitamin B is implicated in reducing the risks of hyperhomocysteinemia, which is a risk factor for coronary heart disease. Though the mechanism of this is not known, there are studies that indicate that vitamin deficiencies and deficiencies in minerals iron and zinc are equivalent to radiation damage to DNA. These deficiencies result in breaks or lesions in the DNA strands. These breaks are due to single or base pair excisions or the underdevelopment of uracil. The result is that the incidence of cancer is high in patients whose nutritional intake does not meet the recommended amounts of fruits and vegetables. These low intakes can also accelerate the process of aging.

In addition to micronutrients, macronutrients are also important. These are fats, carbohydrates and proteins. An unnatural balance in the intake of macronutrients can give rise to several common diseases. The Atkins diet is now very popular. It essentially believes that since proteins is not efficiently metabolized by the body; most of it is discarded into uric waste. The diet avoids carbohydrates, which has been the mainstay of most previously held beliefs. This belief is founded on the fact that Americans do not exercise because of the nature of the culture. Any carbohydrates not used in metabolism are converted from glucose to glycogen and stored in the liver. Meat consumption has been identified with risks of certain diseases because of the fat content. The process of cooking is also believed to change to composition of meat creating, in the process, certain carcinogens. (Kaput & Rodriguez, 2004)

One of the most common diseases that appear to afflict many Americans is type-2 diabetes. A disease progress is marked by a progression from a healthy phenotype to a diseased phenotype. Type 2 diabetes develops when after insulin resistance and pancreatic beta cell failures. This probably occurs by a change in gene expression or metabolic changes in the gene products. Type-2 diabetes is a good example of how diet can affect the genotype. Obesity, excess sugar and fat in the diet are all contributory factors. Other factors are alcoholism, dyslipidemia, cardiovascular disease and other metabolic syndrome. Certain minorities such as African-Americans are also more predisposed to being affected by diabetes. Type-2 diabetes is an interesting test case for Nutrigenomics because diet restrictions and exercise can reduce the symptoms. This means that environmental factors can change the genomic factors. And yet others need medications to reduce symptoms. This is called phenotypic plasticity, which also involves reversing the progress of the disease by controlling the environment. Most other diseases do not show such phenotype plasticity. All of the co-factors of diabetes are associated with excess fat in the tissues. This means that there is a strong correlation with fat in the system and diabetes 2. Studies have shown that excess far of acyl coenzyme A is associated with insulin resistance.

Diabetes can be reduced through a diet that can decrease the role of insulin in the synthesis and storage of fat and also decrease fatty acid oxidation. In attempting to understand the role of fat metabolism and diabetes, a diet consisting of long-range omega fatty acids has been shown to decrease the role of influence in fatty acids. It has also been shown that certain high-glycemic carbohydrates such as sugars and starches help, through low fat high-carbohydrate diets are not helpful. However, not everyone even with a high fatty and carbohydrate diet suffers from diabetes. These individuals are resistant to the genetic conditions that cause the malfunctions that result in insulin resistance and diabetes mellitus. Therefore there are ample opportunities to study Nutrigenomics associated with diabetes. Researchers have suggested that not a gene but a mechanistic pathway approach would better serve identifying the… [END OF PREVIEW]

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