title: Hepatic lipase activity during oral and parenteral 17 beta-estradiol replacement therapy: high-density lipoprotein increase may not be antiatherogenic.
abstract: OBJECTIVE
  Hepatic lipase activity is involved in the removal of cholesterol and phospholipid from plasma high-density lipoprotein (HDL) to the liver. Changes in hepatic lipase are responsible for some lipoprotein modifications observed during estrogen administration (i.e., increased HDL levels). The aim of this study was to compare the effects of alternative routes of administration of estrogen on hepatic lipase activity and lipoprotein metabolism.
  
  
  METHODS
  The effects of oral and parenteral estradiol (E2) replacement therapy on post-heparin hepatic lipase were studied in the short-term (6 weeks) in postmenopausal women.
  
  
  METHODS
  Ten patients received 2 mg/d or oral micronized E2 and 10 patients 3 mg/d of percutaneous E2.
  
  
  RESULTS
  Both treatments significantly increased plasma E2 levels. Hepatic lipase decreased (-33%) significantly (P less than 0.05), and the phospholipids and free cholesterol content of HDL and HDL3 increased significantly (P less than 0.05) during oral but not during parenteral treatment.
  
  
  CONCLUSIONS
  The short-term pharmacological effect of E2 on hepatic lipase depends on the route of administration. The inhibition of this enzyme may reduce the removal of HDL-cholesterol by the liver. The expected vascular benefits of such a pharmacological increase in HDL are questionable.
authors.affiliation: Department of Internal Medicine and Nutrition, Hôtel Dieu, Paris, France.
authors.forename: A
authors.initials: A
authors.lastname: Basdevant
authors.forename: B
authors.initials: B
authors.lastname: de Lignieres
authors.forename: P
authors.initials: P
authors.lastname: Simon
authors.forename: D
authors.initials: D
authors.lastname: Blache
authors.forename: G
authors.initials: G
authors.lastname: Ponsin
authors.forename: B
authors.initials: B
authors.lastname: Guy-Grand
mesh_terms: D000279:Administration, Cutaneous; D000284:Administration, Oral; D000704:Analysis of Variance; D001053:Apolipoproteins / Q000097:blood; D001161:Arteriosclerosis / Q000517:prevention & control; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D004958:Estradiol / Q000008:administration & dosage / Q000097:blood / Q000627:therapeutic use*; D015914:Estrogen Replacement Therapy; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D006801:Humans; D007527:Isoenzymes / Q000097:blood*; D008049:Lipase / Q000097:blood*; D008075:Lipoproteins, HDL / Q000097:blood*; D008099:Liver / Q000201:enzymology*; D007986:Luteinizing Hormone / Q000097:blood; D008593:Menopause; D010743:Phospholipids / Q000097:blood
chemical_list: D001053:Apolipoproteins; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D007527:Isoenzymes; D008075:Lipoproteins, HDL; D010743:Phospholipids; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D002784:Cholesterol; D008049:Lipase