title: Growth hormone induces low-density lipoprotein clearance but not bile acid synthesis in humans.
abstract: OBJECTIVE
  Growth hormone (GH) induces hepatic low-density lipoprotein (LDL) receptors and lowers plasma cholesterol. We characterized the influence of GH treatment on plasma LDL clearance in normal humans and investigated the relative role of LDL receptor (LDLR) activity and stimulation of bile acid synthesis in subjects with different LDLR expression.
  
  
  RESULTS
  Plasma clearance of autologous 125I-LDL was measured before and during 3 weeks of treatment with GH (0.1 IU/kg per day) in 9 healthy young males. Plasma LDL cholesterol was reduced by 13% and the fractional catabolic rate of LDL increased by 27%. More marked changes were seen in a patient with hypopituitarism substituted with GH (0.07 IU/kg per day) for 3 months. In a second study, GH dose-dependently reduced LDL cholesterol and increased Lp(a) levels in 3 groups of males: younger and elderly healthy subjects and heterozygous familial hypercholesterolemia (FH). No effect on bile acid synthesis measured by the plasma marker 7alpha-hydroxy-4-cholesten-3-one was observed. In an LDLR-deficient FH homozygote, LDL cholesterol was not affected by GH.
  
  
  CONCLUSIONS
  GH treatment reduces plasma LDL cholesterol by inducing LDL clearance. In humans, LDLR expression is a prerequisite for this effect, whereas it is not related to stimulation of bile acid synthesis.
authors.affiliation: Metabolism Unit, Center for Metabolism and Endocrinology, Department of Medicine, Novum, Sweden.
authors.forename: Suzanne
authors.initials: S
authors.lastname: Lind
authors.forename: Mats
authors.initials: M
authors.lastname: Rudling
authors.forename: Sverker
authors.initials: S
authors.lastname: Ericsson
authors.forename: Hans
authors.initials: H
authors.lastname: Olivecrona
authors.forename: Mats
authors.initials: M
authors.lastname: Eriksson
authors.forename: Birgit
authors.initials: B
authors.lastname: Borgström
authors.forename: Gösta
authors.initials: G
authors.lastname: Eggertsen
authors.forename: Lars
authors.initials: L
authors.lastname: Berglund
authors.forename: Bo
authors.initials: B
authors.lastname: Angelin
mesh_terms: D000328:Adult; D000069059:Atorvastatin; D001647:Bile Acids and Salts / Q000096:biosynthesis*; D002648:Child; D008078:Cholesterol, LDL / Q000097:blood / Q000378:metabolism / Q000652:urine; D003084:Colestipol / Q000627:therapeutic use; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D004359:Drug Therapy, Combination; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use; D006579:Heterozygote; D019382:Human Growth Hormone / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D006938:Hyperlipoproteinemia Type II / Q000097:blood / Q000188:drug therapy / Q000378:metabolism / Q000652:urine; D007018:Hypopituitarism / Q000097:blood / Q000378:metabolism / Q000652:urine; D008077:Lipoproteins, LDL / Q000097:blood / Q000378:metabolism* / Q000652:urine; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000627:therapeutic use
chemical_list: D001647:Bile Acids and Salts; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D008077:Lipoproteins, LDL; D011758:Pyrroles; D019382:Human Growth Hormone; D000069059:Atorvastatin; D003084:Colestipol