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Apoprotein-e-rich high-density lipoproteins inhibit ovarian androgen synthesis

Academic Article
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Overview

authors

  • Dyer, C. A.
  • Curtiss, Linda

publication date

  • August 1988

journal

  • Journal of Biological Chemistry  Journal

abstract

  • The influence of high density lipoproteins (HDL) on luteinizing hormone-stimulated rat ovarian theca/interstitial cell steroidogenesis was studied. Without HDL the cells produced primarily androgens from progestin precursors. In the presence of rat or human HDL steroid output increased 3-5-fold, but the type of steroid produced was dependent on the source of the HDL. Human HDL nonselectively amplified luteinizing hormone-stimulated steroid production, whereas rat HDL promoted progestin production without a concomitant increase in androgen output. Comparisons of the activities of apoprotein E-rich HDL (e.g. HDL from intact mature rats) with apoprotein E-poor HDL (e.g. human HDL or rat HDL from hypophysectomized immature rats) suggested that apoprotein E was responsible for the inhibition of androgen production. Furthermore, the inhibitory activity of rat HDL was abolished by depleting apoprotein E-containing lipoproteins with heparin affinity chromatography. Direct evidence that apoprotein E was the inhibitory constituent of rat HDL was obtained by showing that isolated lipid-free rat apoprotein E inhibited androgen production, whereas isolated rat apoproteins A-I and A-IV did not. The possible paracrine function of apoprotein E in ovarian follicular maturation of the ovary is discussed.

subject areas

  • Androgens
  • Animals
  • Apolipoproteins E
  • Cells, Cultured
  • Female
  • Humans
  • Hypophysectomy
  • Kinetics
  • Lipoproteins, HDL
  • Male
  • Ovary
  • Rats
  • Rats, Inbred Strains
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Identity

International Standard Serial Number (ISSN)

  • 0021-9258

PubMed ID

  • 3392050
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Additional Document Info

start page

  • 10965

end page

  • 10973

volume

  • 263

issue

  • 22

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