Questi sono solo alcuni degli articoli che ho trovato, ma dicono tutti la stessa cosa... Peccato ne avevo trovato uno che spiegava esattamente la distribuzione dei due isoenzimi nel corpo umano ma non lo ritrovo più....
http://www.medscape.com/viewarticle/410576
MPB does not occur in men with a genetic deficiency of type II 5 alpha-reductase, which converts testosterone to dihydrotestosterone (DHT).[5] Type I 5 alpha-reductase isoenzyme is present in the skin.[6] The type II isoenzyme is present in hair follicles and the prostate.[6,7] The genes encoding type I and type II 5 alpha-reductase isoenzymes are not associated with male pattern baldness.[4] The clinical pattern of hair loss is apparently the result of genetically determined distribution of androgen-sensitive hair follicles transformed from terminal to miniaturized follicles.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=294929
There was no qualitative difference in 5 alpha-reductase type 1 expression between adult balding vs. nonbalding scalp. The type 2 isozyme is transiently expressed in skin and scalp of newborns. Type 2 is the predominant isozyme detectable in fetal genital skin, male accessory sex glands, and in the prostate, including benign prostatic hyperplasia and prostate adenocarcinoma tissues. Both isozymes are expressed in the liver, but only after birth. These results are consistent with 5 alpha-reductase type 1 being responsible for virilization in type 2-deficient subjects during puberty, and suggest that the type 2 isozyme may be an initiating factor in development of male pattern baldness.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10583052&dopt=Abstract
In contrast, in scalp cryosections stained with antibody to 5aR1, no immunostaining was observed within hair follicles. Intense staining for the type 1 isozyme was, however, detected within sebaceous glands. Our immunolocalization data suggest that the results seen in clinical trials of men with male pattern hair loss treated with finasteride may be due, at least in part, to local inhibition of 5aR2 within the hair follicle