Abstract
Multiple studies have demonstrated a role for scavenger receptor class B type 1 (SR-B1) in female fertility. Recent studies have implicated specific SR-B1 gene polymorphisms in decreased progesterone production and suboptimal fertility outcomes. The lipoprotein receptor SR-B1 has been known to mediate selective uptake of lipids into steroidogenic tissues such as the ovaries. SR-B1 plays a major role in the ability of the corpus luteum to produce progesterone, which is known to play a key role in sustaining early pregnancy. Animal studies have demonstrated that deficiency in SR-B1 results in subfertility that can be restored with addition of SR-B1 function. Single-nucleotide polymorphisms in SCARB1, the gene encoding SR-B1, have been associated with human lipid levels. Women undergoing infertility treatment with low SR-B1 expression in granulosa cells were noted to have plasma estradiol levels half the normal levels and a significantly lower number of retrieved oocytes. In vitro, deficiency of SR-B1 is associated with lower progesterone secretion in human granulosa cells. Certain SR-B1 polymorphisms have been associated with lower follicular progesterone levels and a significantly lower clinical pregnancy rate. Deficiency of SR-B1, particularly due to single-nucleotide polymorphisms, could explain some features of female human infertility.
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