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December 1, 2001Journal of Clinical InvestigationOpen Access

Abnormal lipoprotein metabolism and reversible female infertility in HDL receptor (SR-BI)–deficient mice

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Why the study?

Does modifying abnormal HDL structure and quantity via apoA-I inactivation or probucol treatment restore fertility in SR-BI-deficient female mice?

Population

Female HDL receptor-deficient knockout mice, wild-type mice, apoA-I KO mice, SR-BI/apoA-I double-KO mice…

Comparison

Genetic disruption of the apoA-I gene or… vs Untreated SR-BI KO mice, wild-type mice, or sham…

Design

Preclinical

Follow-up

1 to 4 months

Authors

HMHelena E. MiettinenUniversity of HelsinkiHRHelen RayburnHoward Hughes Medical InstituteMKMonty KriegerMassachusetts Institute of Technology

Discussion

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Implication

Suggests HDL modification as a reversible infertility target in animal models; leaves open whether probucol or similar agents warrant human investigation.

Structured PICO

Does modifying abnormal HDL structure and quantity via apoA-I inactivation or probucol treatment restore fertility in SR-BI-deficient female mice?

P
Population
Female HDL receptor (SR-BI)-deficient knockout mice, wild-type mice, apoA-I KO mice, SR-BI/apoA-I double-KO mice, RAG-2 KO mice, and SR-BI/RAG-2 double-KO mice.
I
Intervention
Genetic disruption of the apoA-I gene or administration of the cholesterol-lowering drug probucol (0.5% wt/wt in chow) for 1-3.5 weeks before mating and throughout the experiment; or ovary transplantation into RAG-2 KO hosts.
C
Comparator
Untreated SR-BI KO mice, wild-type mice, or sham ovary transplantation.
O
Outcome
Fertility, measured as the percentage of females producing litters and the average number of pups delivered per month per female mated.

Abnormal lipoprotein metabolism causes reversible female infertility in SR-BI-deficient mice, which can be restored by modifying HDL structure or quantity.

Limitations

  • Mixed genetic backgrounds may introduce unknown modifier alleles
  • The exact mechanism by which probucol lowers murine plasma cholesterol and modifies lipoproteins is undefined

Cite This Study

Miettinen et al. (2001) studied this question.

synapsesocial.com/papers/6a89d2ea439f8b7e01433c24https://doi.org/10.1172/jci13288
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Pre-β-HDL stimulates placental lactogen release from human trophoblast cells1999 · 9 citations
  2. 2Dissociation of tissue uptake of cholesterol ester from that of apoprotein A-I of rat plasma high density lipoprotein: selective delivery of cholesterol ester to liver, adrenal, and gonad.1983 · 492 citations
  3. 3Targeted mutation of plasma phospholipid transfer protein gene markedly reduces high-density lipoprotein levels1999 · 405 citations
  4. 4Normal plasma lipoproteins and fertility in gene-targeted mice homozygous for a disruption in the gene encoding very low density lipoprotein receptor.1995 · 255 citations
  5. 5Overexpression of Human Lecithin Cholesterol Acyltransferase Leads to Hyperalphalipoproteinemia in Transgenic Mice1995 · 128 citations