The skin lipids play important roles in the epidermal function
such as cell growth and differentiation, energy metabolism, signal transduction and structural components for cells [33]. Lipid
metabolism is thought to play an essential role in lipid envelope
of hair and skin, but also involvement in hair development and
function. In animal models, genetic errors in lipid metabolism cause
both inflammation and abnormal hair growth, resembling several
dermatological disorders [34]. The Elovl3 gene product, which
belongs to a highly conserved family of microsomal enzymes
involved in the formation of very long chain fatty acids, revealed a
distinct expression in the skin that was restricted to the sebaceous
glands and the epithelial cells of the hair follicles. The Elovl3-ablated
mice displayed a sparse hair coat [5]. Insig-1 and Insig-2, two closely
related proteins, are essential for feedback inhibition of cholesterol
biosynthesis. Insig-double knockout (Epi-Insig-DKO) mice exhibit
defects in hair growth along with other skin abnormalities, including
hyperkeratosis [6]. The acyl-CoA binding protein (Acbp), which
binds long-chain fatty acyl-CoA esters, is essential for fatty acyl-CoA
transport and pool formation. Deletion of Acbp in mouse results in
sebocyte hyperplasia and sparse, matted hair with a greasy
appearance [35]. Fatty acid transport protein (FATP) 4 is the primary
intestinal FATP and is thought to play a major role in dietary fatty
acid uptake. Mutation in FATP4 also defects in hair follicle
morphogenesis and hair growth [36]. Opportunities for pharmacological
intervention in hair disorders may be derived from new
knowledge about lipid metabolism [34