Acyl-CoA Dehydrogenases

01/01/1984 - "Two sibs with the acute neonatal form of glutaric aciduria type II (deficient in vivo activity of multiple acyl-CoA dehydrogenases) are described. "
12/01/1980 - "Glutaric aciduria type II: in vitro studies on substrate oxidation, acyl-CoA dehydrogenases, and electron-transferring flavoprotein in cultured skin fibroblasts."
11/01/1994 - "Organic acid urinalysis was consistent with the diagnosis of multiple acyl-CoA dehydrogenase deficiency or glutaric acidemia type II. In cultured lymphoblastoid cells from this patient there was impaired beta-oxidation, but the activities of acyl-CoA dehydrogenases were normal. "
07/01/1986 - "He had glutaric aciduria type II, and his cultured fibroblasts contained normal activity of four different acyl CoA dehydrogenases, but there was deficiency of electron transfer flavoprotein:ubiquinone oxidoreductase (ETF-QO). "
06/15/2010 - "Glutaric aciduria type 2 (multiple acyl-CoA dehydrogenase deficiency, MAD) is a multiple defect of mitochondrial acyl-CoA dehydrogenases due to a deficiency of electron transfer flavoprotein (ETF) or ETF dehydrogenase. "

05/15/2005 - "In the current study, an in vivo rat model of myocardial ischemia was utilized to determine whether specific acyl-CoA dehydrogenases exhibit ischemia-induced alterations in activity, identify mechanisms responsible for changes in enzyme function, and assess the effects on mitochondrial respiration. "

12/01/2017 - "An elevated blood concentration of nonesterified fatty acids is one of the indicators of NEB in cattle among others like increased β-hydroxy butyrate concentration, and decreased concentrations of glucose, insulin, and insulin-like growth factor-I. Assuming that liver carnitine concentrations might limit hepatic fatty acid oxidation capacity in dairy cows, further study of the role of acyl-CoA dehydrogenases and/or riboflavin in bovine ketosis is warranted."

05/15/2005 - "In the current study, an in vivo rat model of myocardial ischemia was utilized to determine whether specific acyl-CoA dehydrogenases exhibit ischemia-induced alterations in activity, identify mechanisms responsible for changes in enzyme function, and assess the effects on mitochondrial respiration. "

09/01/1994 - "Inherited defects of acyl-CoA dehydrogenases occur in humans, and MCAD deficiency is the most common. "
10/30/2023 - "Furthermore, a noticeable reduction in different Acyl-CoA-dehydrogenases was detected (VLCAD-deficiency p < 0.05, MCAD-deficiency p = 0.07). "
01/01/1988 - "Assay of acyl-CoA dehydrogenases in muscle and liver and identification of four new cases of medium-chain acyl-CoA dehydrogenase deficiency associated with systemic carnitine deficiency."
01/13/1995 - "Matrix enzyme deficiencies, such as medium- and short-chain acyl-CoA dehydrogenases, were characterized by elevated concentrations of intermediates corresponding to their respective substrates (octanoyl- and decenoylcarnitines in medium-chain acyl-CoA dehydrogenase deficiency and butyrylcarnitine in short-chain acyl-CoA dehydrogenase deficiency). "