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Wednesday, August 9, 2017

All About Vitamins: High Dose of Vitamin B2 for Treatment of Defective Gene ACAD9

Kyle J. Norton(Scholar, Master of Nutrients), all right reserved.
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
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Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.

High dose of supplement of riboflavin may have a beneficiary effect for patients with gene ACAD9 defected, a renowned institute reported.

Vitamin B2 also known as Riboflavin, is a water-soluble, yellow-orange organic compound found abundantly in milk, meat, eggs, nuts, enriched flour, green vegetables, etc. The vitamin is essential for normal cellular growth and function and best known for converting energy from protein, fat, and carbohydrates during metabolism and its antioxidant effects in oxidation-reduction reactions.

Gene ACAD9 provides function of making enzyme in the mitochondria, by converting oxygen and nutrients to energy involved structures inside cells.

In a reported study, high dose of  riboflavin treatment of a 13-year-old boy reduced symptoms of exercise intolerance, weakness, and mild psychomotor delay and muscle histochemistry with severe complex I deficiency due to mitochondrial proliferation caused by ACAD9 defected

According to the Clinical Genomics Unit, Maastricht University, oxidative phosphorylation defect due to ACAD9 defected, decreased function in production and modification of the enzymes, including arginine-532 into tryptophan, induced mitochondrial complex I deficiency.

More importantly, the study also found that mutation of gene to activate protein in production of enzymes is found to be absent in 188 ethnically matched healthy controls.

Dr. Gerards M, the lead author said,"Protein modelling suggested a functional effect due to the loss of a stabilizing hydrogen bond in an α-helix and a local flexibility change. " and
"fibroblasts of patients with wild-type and mutant ACAD9. Wild-type, but not mutant, ACAD9 restored complex I activity".

The astonished findings suggested that gene expression may become important for further studies as ACAD9 defected in complex I function can be improved by intake of high dose of Vitamin B2.


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Sources
(1) Riboflavin-responsive oxidative phosphorylation complex I deficiency caused by defectiveACAD9: new function for an old gene by Gerards M1, van den Bosch BJ, Danhauser K, Serre V, van Weeghel M, Wanders RJ, Nicolaes GA, Sluiter W, Schoonderwoerd K, Scholte HR, Prokisch H, Rötig A, de Coo IF, Smeets HJ.(PubMed)
(2) Garone C, Donati MA, Sacchini M, et al. Mitochondrial encephalomyopathy due to a novel mutation in ACAD9. JAMA Neurol. 2013;70(9):1177–1179. [PubMed]

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