Acetyl-CoA carboxylase is a biotin-dependent enzyme that catalyzes the irreversible carboxylation of acetyl-CoA to produce malonyl-CoA. Malonyl-CoA inhibits the rate-limiting step in beta-oxidation of fatty acids. Malonyl-CoA inhibits fatty acids from associating with carnitine by regulating the enzyme carnitine acyltransferase.
Biotin supplementation would then both inhibit beta-oxidation and assist with chain elongation in fatty acid biosynthesis.
I have been arguing that increases is beta-oxidation that result from increased intakes of polyphenols can lead to difficulties in schizophrenia. Given the dual functions of malonyl-CoA in inhibiting beta-oxidation and assisting with fatty acid elongation if there is excessive beta-oxidation there could be difficulties in fatty acid elongation. Supplemental biotin would decrease beta-oxidation and increase fatty acid elongation which would be headed in the right direction. Biotin would not be supplemented at the same time as pantothenic acid as pantothenic acid is a competitive inhibitor of biotin transport.