A Computational Model of Mitochondrial Beta-Oxidation Highlighting the Implications on Uremia Disease in Human
Abhishek Sengupta1, Sarika Saxena2
1Abhishek Sengupta, Amity Institute of Biotechnology, Amity University, Noida, India.
2Sarika Saxena, Amity Institute of Biotechnology, Amity University, Noida, India.
Manuscript received on December 08, 2014. | Revised Manuscript received on December 15, 2014. | Manuscript published on January 05, 2014. | PP: 188-192 | Volume-3 Issue-6, January 2014. | Retrieval Number:F2043013614/2014©BEIESP
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© The Authors. Published By: Blue Eyes Intelligence Engineering and Sciences Publication (BEIESP). This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)
Abstract: Enzyme deficiencies can segment the metabolic reactions in the mitochondrion and may spark to augmentation of specific substrates causing severe clinical manifestations. During the state of starvation mitochondrial oxidation of long-chain fatty acids procures a vital source of energy for the heart as well as for skeletal muscle. A computational kinetic network of reactions, compounds and parameters was constructed to correlate the mitochondrial fatty acid beta-oxidation to disease conditions. Carnitine deficiency limits the availability of the long chain acyl-CoAs inside the mitochondrial matrix. Majorly, carnitine is necessary for fatty acid transport to sites of beta-oxidation in the mitochondria. An increased ratio of long-chain acyl-carnitine (LCAC) to free carnitine, was observed when carnitine level was declined. This verifies that uremic patients have altered carnitine metabolism. Subjecting the constructed model of the biochemical reactions involved in fatty acid catabolism to further simulations at varying concentrations will provide predictive models to identify the disease targets.
Keywords: Mitochondrial Beta-Oxidation, Carnitine Deficiency, Computational Model, Uremia.