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The epigenetics of high fructose corn syrup at a molecular level may be explained under several principles, but two of many principles seem to be the major ones. The energy intake and its expenditure regulations are the key determinants of the epigenetics of high fructose in the body. This single most principle of energy intake and expenditure integrates with other important molecular processes, especially that of transportation and concentration of substrates over or across tissues and/or tissue membranes. Normally, the proper functioning of the body cells depends on the maintaining of an optimal concentration of the blood sugars, which includes fructose, glucose, and galactose.
The role and functions of maintaining the optimal stabilized blood sugar level are designated to certain body organs such as the kidney and the liver which deals mostly with the regulation of glucose in the blood. The tissues of these two body organs play an important role in producing and exportation of glucose, hence, keeping a stable blood sugar level. Increasing or decreasing the amount of glucose concentration level in the blood, directly affects the concentration of fructose in blood, since they all act as determinants of the overall blood concentration (Johnson and Timothy 125)
In this case, high fructose corn syrup in the body may result from the dysfunction of metabolic processes of monosaccharide glucose or fructose molecules. Any activity or substance that would affect negatively the phosphorylation of fructose, hence, preventing the fructose molecules from entering into the phosphorylation process would lead to the high concentration of fructose in the blood tissues.
This will mostly happen especially when the production process of the enzyme fructokinase or the enzyme itself is altered such that it cannot initiate the metabolic reactions of fructose. While we recognize the liver tissues as the site where large quantities of energy are produced, and the site where fructokinase activities take place, high fructose concentration occurs at the portal blood tissues due to dysfunction of the tissues of the liver which are accountable and responsible for the role of fructose removal that allows the uptake of it from the gut membrane tissues (Cox, Doudna, and O’Donnell 46).
In the liver tissues and cells, high fructose concentrations will be realized when blockage or alteration of the glycolytic process after consumption of large quantities of fructose-containing foods. When glycolytic processes are thwarted at the liver tissues, this prevents the utilization of fructose in the promotion of the synthesis of fats. The failure of the synthetic process to produce its final products related to the utilization of fructose in the body ultimately leads to an increased concentration of fructose in the blood tissues in circulation. It implies that a high level of fructose substrate would be made available within the body tissues through the elimination of all other essential substrates and factors necessary for the production of fatty material in the body (Hu 65).
Moreover, fructose concentration in the body cells/ blood tissues can be regulated through the control of enzymatic substrate production level. This may happen with the control of insulin enzymes which tell the level of glucose concentration in the blood tissues and subsequently stimulate the redirecting of excess fructose substrate to the process of fatty acid synthesis. Methylation of the genetic materials responsible for the production of insulin would affect the cells responsible for the production of insulin. The resultant effect from this is a reduced amount of insulin produces, which will interfere with the detection of the glucose level and therefore the stimulating of directing the fructose substrates into lipid synthesis. The hormone leptin is another way through which high fructose concentration in the body may be regulated.
This is an important hormone endowed with the function of regulating energy release and consumption in the body. As an adipose signal, it regulates the amount of glucose being consumed in the body and thus, its function is intimately related to the control of the blood sugars concentration including fructose (Cox, Doudna, and O’Donnell 234).
Inclusion, the epigenetics of high fructose in the body is mainly achieved through metabolic processes and transportation of substrates across the molecular materials. This may be attained by turning off the phosphorylation processes and the genetic process of producing enzyme insulin.
Works cited
Cox, Michael, Jennifer Doudna, and Michael O’Donnell. Molecular Biology Principles and Practice. WH: Freeman, 2007. Print.
Hu, Frank. Obesity epidemiology. New York: Oxford University Press, 2008. Print.
Johnson, Richard, and Gower Timothy. The Sugar Fix: The High-Fructose Fallout That Is Making You Fat and Sick. Rodale Books, 2008. Print.
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