ACAD-12 Activators

Chemical activators of acyl-Coenzyme A dehydrogenase family, member 12 (ACAD12) can facilitate the enzyme's role in catalyzing the initial step of fatty acid β-oxidation. Palmitoyl CoA, as a substrate, directly triggers the activity of ACAD12, enabling the enzyme to perform its dehydrogenation function. Similarly, oleic acid is another substrate that directly engages with ACAD12 to initiate the oxidation process. On the other hand, malonyl CoA influences ACAD12 activity by allosteric regulation, which is a form of indirect activation, where the presence of malonyl CoA signals the necessity for fatty acid degradation and thus enhances the enzyme's function. Nicotinamide adenine dinucleotide (NAD+) is crucial for ACAD12's activity, serving as an essential cofactor that the enzyme requires to carry out the dehydrogenation of fatty acyl-CoA compounds. Without NAD+, ACAD12 would be unable to perform its catalytic action.

Apart from direct substrates and essential cofactors, several compounds assist in the indirect activation of ACAD12. L-Carnitine plays a pivotal role in transporting fatty acids into the mitochondria, thereby ensuring that ACAD12 has a continuous supply of substrates to act upon. Coenzyme Q10 participates in the electron transport chain by accepting electrons from ACAD12, which is vital for the regeneration of the enzyme's active state. Vitamin C contributes to maintaining the redox state within the cell, which supports the optimal functioning of ACAD12. Alpha-Lipoic acid and riboflavin are also involved in the enzyme's activation; alpha-lipoic acid aids in the recycling of cofactors necessary for ACAD12, while riboflavin, as a precursor to flavin adenine dinucleotide (FAD), is integral to ensuring proper electron transfer during the enzyme's catalysis. Succinic acid and pantothenic acid (Vitamin B5) bolster the enzyme's function indirectly; succinic acid by being part of the tricarboxylic acid cycle that produces essential reducing equivalents, and pantothenic acid by contributing to the synthesis of Coenzyme A, which is necessary for the formation of acyl-CoA substrates. Finally, acetyl-CoA, although not a direct substrate for ACAD12, can modulate the enzyme's activity by its involvement in various intersecting metabolic pathways.