2001
DOI: 10.1172/jci13288
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Abnormal lipoprotein metabolism and reversible female infertility in HDL receptor (SR-BI)–deficient mice

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Cited by 162 publications
(114 citation statements)
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“…Total E 2 levels were normal in Scarb1-null females, therefore discarding the disruption of this hormonal axis as a major factor for the gender-specific bone alterations. Though female Scarb1-null females show reduced fertility (Miettinen et al 2001), their ovarian functions are normal in terms of progesterone and E 2 production (Rigotti et al 2003), indicating existing compensatory mechanisms in some aspects. Moreover, HDL carries a large proportion of esterified estrogens in the bloodstream (Hockerstedt et al 2002); it is unknown whether Scarb1 deficiency impacts the distribution of E 2 esters vs free E 2 .…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Total E 2 levels were normal in Scarb1-null females, therefore discarding the disruption of this hormonal axis as a major factor for the gender-specific bone alterations. Though female Scarb1-null females show reduced fertility (Miettinen et al 2001), their ovarian functions are normal in terms of progesterone and E 2 production (Rigotti et al 2003), indicating existing compensatory mechanisms in some aspects. Moreover, HDL carries a large proportion of esterified estrogens in the bloodstream (Hockerstedt et al 2002); it is unknown whether Scarb1 deficiency impacts the distribution of E 2 esters vs free E 2 .…”
Section: Discussionmentioning
confidence: 99%
“…003379; Bar Harbor, ME, USA) and crossbred with WT C57BL/6 mice. Owing to their low fertility, Scarb1-null females were fed a 0.5% probucol diet (Research Diet, New-Brunswick, NJ, USA) for 10 days before mating (Miettinen et al 2001). The heterozygous (HZ) progeny was mated to obtain first generation (F1) WT and null couples; HZ, WT, and null couples were bred in parallel throughout each generation to allow littermate and inter-litter comparisons, as well as to insure that probucol did not affect the observed phenotype.…”
Section: Animalsmentioning
confidence: 99%
“…Interestingly, another major phenotypic feature of murine SR-BI deficiency is female, but not male, infertility, which was associated with decreased in vitro viability and development of preimplantational embryos from SR-BI knockout females [57,63]. The abnormal ␣-tocopherol metabolism in SR-BI-deficient mice may provide some insights into the underlying mechanism(s) that could explain this phenotype.…”
Section: Potential Pathophysiological Relevance Of Sr-bimediated ␣-Tomentioning
confidence: 99%
“…However, dietary ␣-tocopherol supplementation did not reverse the fertility defect of SR-BI knockout females (Mardones et al, unpublished data), which is consistent with an essential role of SR-BI in delivering ␣-tocopherol to ovaries. In contrast, the antioxidant probucol restored fertility in SR-BI-deficient female mice [63]. Further studies are required to establish whether abnormal membrane lipoperoxides and/or protein and DNA oxidative damage due to decreased vitamin E content play a role in determining oocyte dysfunction that leads to abnormal in vitro development of preimplantational embryos in SR-BIdeficient females.…”
Section: Potential Pathophysiological Relevance Of Sr-bimediated ␣-Tomentioning
confidence: 99%
“…SR-B1 has been implicated in protection of female fertility, and homozygous SR-BI KO females have abnormal HDLs, ovulate dysfunctional oocytes, and are infertile (Miettinen et al, 2001). A recent study shown that SR-B1 expression in extra embryonic tissues was involved in the maternal-fetal transport of cholesterol and/or other lipids with a role during neural tube http://dx.doi.org/10.1016/j.acthis.2015.03.007 0065-1281/© 2015 Elsevier GmbH.…”
Section: Introductionmentioning
confidence: 99%