Hair growth cycle is arrested in SCD1-deficiency by impaired Wnt3a-palmitoleoylation and retrieved by artificial lipid barrier.

J Invest Dermatol. 2017 Mar 1. pii: S0022-202X(17)31158-2. doi: 10.1016/j.jid.2017.02.973. [Epub ahead of print]
Hair growth cycle is arrested in SCD1-deficiency by impaired Wnt3a-palmitoleoylation and retrieved by artificial lipid barrier.

Stoffel W1, Schmidt-Soltau I2, Jenke B2, Binczek E2, Hammels I3.

Stearoyl-CoA desaturase 1 (SCD1) is the dominant member of the SCD-isozyme family, regarded as a major regulator of lipid and energy metabolism in liver and adipose tissue. SCD1-deficiency impairs the desaturation of de novo-synthesized palmitoyl- and stearoyl-CoA to palmitoleoyl- and oleoyl- CoA. Scd1-/- mice develop metabolic waste syndrome and skin lesions: epidermal barrier disruption, alopecia and degeneration of sebaceous glands. The unifying molecular link between the two divergent traits remains incompletely understood. Here we show the absence of palmitoleic acid (9Z-16:1) in the lipidome of the scd1-null mouse, that prohibits posttranslational O-palmitoleoylation of Wnt3a-protein, essential for Wnt3a/ß-catenin signaling in stem cell lineage decision in development of the epidermal barrier, hair growth cycle, and sebaceous glands. Substitution of the disrupted epidermal lipid barrier by an inert hydrocarbon coat prevents excessive transepidermal water loss, normalizes thermogenesis and metabolic parameters, and surprisingly leads to the activation of hair bulge progenitor cells and reprograming of a regular hair growth cycle and development of a regular fur in scd1-/- mice. Progenitor sebocytes are not activated. Independent of age, application or removal of the artificial lipid barrier allows the reversible telogen-anagen reentry and exit of the hair growth cycle.

anything we can do about this?

Benjamin Button wrote:anything we can do about this?

Maybe.

Stearoyl-CoA desaturase is a product of Palmitoleate.

The fatty acid, Palmitoleate is considered as a "lipokine" and it appears to have interesting benefits. The main interest in this is that it is a Wnt activator.

Despite dietary intakes being low (<4% of total energy) palmitoleate is the second most abundant monounsaturated fatty acid in most, but not all, blood lipid pools and notably more abundant in adipose tissue. Thus, compared with other fatty acids, the palmitoleate content of lipid pools must be influenced by endogenous synthesis, which appears to be tissue and depot specific.

Unlike other fatty acids, there is a clear tendency towards compartmentalization and tissue-specific formation of palmitoleate.

Palmitoleate has been shown to improve glucose sensitivity and repress liver fat desposition.

Palmitoleate, produced by Stearoyl-CoA desaturase (SCD), is covalently attached to Wnt proteins and is necessary for Wnt protein secretion and signalling.

Theoretically, if a person has a problem with making Stearoyl-CoA desaturase, they could supplement with Palmitoleic acid. A rich source of this includes sea buckthorn seed oil.

maybe this is why emu oil and lard can help some people, they have the same fatty acid profile as human skin (about 4% Palmitoleic acid.)
Also heard recently that PUFA degrades androgen receptor (hence scalp regrowth and body hair suppression anecdotal reports.)

I'll buy the seabuckthorn stuff next time I've got money.

wow, apparently sea buckthorn oil is 36% palmitoleic acid

I read a lot about the WNT pathway and hair growth. Should we not try to mimic this pathway? Can we get some growth this way?