Chandler Marrs, PhD
From the research on AFLP, we know that a mutation in the mitochondrial enzyme responsible for processing an important mitochondrial transporter evokes some, but not all of the cases of this disease process. Notably, in some women with hyperemesis, the fetus carries the mutation and evokes the vomiting, while mom is simply a heterozygous carrier. The mutation (L-3-hydroxyacyl-CoA dehydrogenase deficiency – LCHAD) involves an enzyme (carnitine palmitoyltransferase I – CPT I) responsible for synthesizing the protein that acts as key transporter for fatty acids across the mitochondrial membrane. The protein involved is called carnitine.