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This Concept Map, created with IHMC CmapTools, has information related to: MCAD, 3-Ketoacyl CoA converted by B-ketoacyl CoA thiolase to fatty acyl CoA, Insufficient B oxidation leads due decreased mitochondrial Acetyl CoA, gluconeogenesis with MCAD unable to compensate for usage, leads to decreased levels of blood glucose, Enoyl CoA reaction releases FADH2, short chain fatty acids activated and diffuse to inner mitochondrial membrane to become fatty acyl CoA, 3-Ketoacyl CoA reaction releases NADH, Rose Bud prior to symptoms was in a Fasting state, increased glucagon:insulin leads to activation of glycogen phosphorylase, fatty acyl CoA medium chain acted on by Medium Chain Acyl CoA dehydrogenase, ETC produces ATP, omega oxidation attempts to oxidize at omega end of fatty acid, unsuccessful, leads to build up of dicarboxylic acids, ATP used for energy in the biochemical functions of Rose Bud, acylcarnatine acted on by CPT-II, decreased mitochondrial Acetyl CoA leads to decreased production of ketone bodies, medium chain fatty acids activated and diffuse to inner mitochondrial membrane to become fatty acyl CoA, Insufficient B oxidation depleted levels of acetyl CoA leads to downregualtion of pyruvate carboxylase, Rose Bud has deficiency in Medium Chain Acyl CoA dehydrogenase, urinary dicarboxylic acids symptoms of Rose Bud, glycolysis in all tissues beside liver attempts to maintain levels of Acetyl CoA, activation of glycogen phosphorylase activates glycogenolysis