Flies have a very straighforward lipid metabolism when compared to humans, but with peculiar highlights. Let’s go through them!
Flies are sterol auxotrophs, meaning that they do not synthesize their own sterols, but rather absorb them (primarily ergosterol) from their main food source, yeast. Fly membranes also contain considerably less sterol than mammalian membranes, being only 18% versus 30%.
In sphingolipids, the length of the sphingoid base is much shorter, generally containing only 12 carbons derived from laurate instead of the 16 carbons from palmitate as in mammals. This gives a sphingoid base alkyl chain of C14 instead of C18, whereas the fatty acyl chain, which is attached by an amide linkage to the sphingoid base, is quite long, with C20 being the major species.
In spite of the differences in structure of fly sphingolipids, and the lower abundance of sterols in fly membranes, sphingolipid- and sterol-rich microdomains have been documented by several authors in Drosophila cells and tissues.
Glycosphingolipids are quite different from their mammalian counterparts in that the core disaccharide consists of Man beta-1–4 Glc beta-1-Cer, aka mactosyl-ceramide, instead of Gal beta-1–4 Glc beta-1-Cer in mammals.
Concerning phospholipids, in the case of flies, PE is the major one, accounting for almost 55% of total phospholipids, where choline is only 20%.
Fatty acids are saturated and monounsaturated, with palmitic, palmitoleic, stearic and oleic being the predominant species. Polyunsaturated fatty acids are low, with just linoleic and alpha-linolenic acid contributing to membrane fluidity.
There are no genes encoding for delta-6/delta-5 desaturases, resulting in the total absence of long chain PUFA. The lack of C20 PUFA makes it a special species that does not require C20 PUFA for formation of eicosanoids and other oxygenated metabolites, which are considered to be of broad physiological significance in animals.
If any of you is working with flies cells or insect cells in general, watch out their lipidomics!