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5-Desaturase,
6-
Desaturase, Stearoyl-Coenzyme A (CoA) Desaturase 1, and
Stearoyl-CoA Desaturase 2 in Rat TestisIn mammalian cells essential polyunsaturated fatty acids
(PUFAs) are converted to longer PUFAs by alternating
steps of elongation and desaturation. In contrast to
other PUFA-rich tissues, the testis is continuously
drained of these fatty acids, as spermatozoa are
transported to the epididymis. Alteration of the germ
cell lipid profile from spermatogonia to condensing
spermatids and mature spermatozoa has been described, but
the male gonadal gene expression of the desaturases,
responsible for the PUFA-metabolism, is still not
established. The focus of this study was to characterize
the expression and regulation of stearoyl-coenzyme A
(CoA) desaturase 1(SCD1), stearoyl-CoA desaturase 2
(SCD2),
5- and
6-
desaturase in rat testis. Desaturase gene expression was
detected in testis, epididymis and separated cells from
seminiferous tubulus using Northern blot analysis. For
the first time SCD1 and SCD2 expression is demonstrated
in rat testis and epididymis, both SCDs are expressed in
epididymis, while testis mainly contains SCD2.
Examination of the testicular distribution of
5- and
6-desaturase and
SCD1 and 2 shows that all four desaturases seem to be
localized in the Sertoli cells, with far lower expression
in germ cells. In light of earlier published results
showing that germ cells are richer in PUFAs than Sertoli
cells, this strengthens the hypothesis of a lipid
transport from the Sertoli cells to the germ cells. As
opposed to what is shown in liver,
5-
and
6-desaturase mRNA levels in
Sertoli cells are upregulated by dexamethasone.
Furthermore, dexamethasone induces SCD2 mRNA. Insulin
also upregulates these three genes in the Sertoli cell,
while SCD1 mRNA is downregulated by both insulin and
dexamethasone.
5- and
6-desaturase, SCD1 and SCD2 are all
upregulated by FSH. A similar upregulation of the
desaturases is observed when treating Sertoli cells with
(Bu)2cAMP, indicating that the desaturase
upregulation observed with FSH treatment results from
elevated levels of cAMP. Finally, testosterone has no
influence on the desaturase gene expression. Thus, FSH
seems to be a key regulator of the desaturase expression
in the Sertoli cell.
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