title: Molecular interactions of natural and synthetic steroids in female hamsters' flank organs.
abstract: BACKGROUND
  The initial step of steroidal action on target cells is gene activation; therefore, the quantification of mRNA is a direct method for comparing the role of different steroids in the skin.
  
  
  OBJECTIVE
  This study demonstrated the role of several steroids on the mRNA expression encoding for different enzymes involved in the lipid metabolism in hamsters' flank organs, which are a pilosebaceous complex.
  
  
  METHODS
  To determine the effect of treatments with testosterone (T) progesterone (P), levonorgestrel (LNG), 17α-p-chlorobenzoyloxy-6-chloropregn-4,6-diene-3,20-dione (5) and 17α-p-chlorobenzoyloxy-4,6-pregnadiene-3,20-dione (6); T and/or LNG; T and 5 or 6; P and/or 5 or 6 on the expression of mRNA encoding for lipid enzymes, the steroids were applied to the glands; later, the mRNAs expression for the enzymes was determined by PCR. The binding of 5 and 6 to the progesterone receptor (PR) was also evaluated.
  
  
  RESULTS
  Treatments with T, LNG, T+LNG, P, T+P, 5, T+5, T+6, P, P+5 and P+6 increased the mRNA expression for glycerol 3-phosphate acyl transferase (GPAT), β-hydroxy-β-methylglutaryl-CoA synthase (HMG-CoA-S), β-hydroxy-β-methylglutaryl-CoA reductase (HMG-CoA-R), phosphatidylinositol synthase as compared to the controls. However, squalene synthase was increased with all treatments except with T+5 and 6; 6 did not significantly increase the expression for GPAT or HMG-CoA-S, however it increased the concentration of HMG-CoA-R enzyme. 5 and 6 bind to the PR, thus indicating that the effect of these steroids on the mRNA expression could be the result of their binding.
  
  
  CONCLUSIONS
  The lipid metabolism is regulated by several steroids thought different mechanism of action, in flank organs.
authors.affiliation: Department of Biological Systems and Animal Production Metropolitan University-Xochimilco, Mexico D.F., Mexico. marisa@correo.xoc.uam.mx
authors.forename: Marisa
authors.initials: M
authors.lastname: Cabeza
authors.forename: Barak
authors.initials: B
authors.lastname: Naranjo
authors.forename: Yvonne
authors.initials: Y
authors.lastname: Heuze
authors.forename: Araceli
authors.initials: A
authors.lastname: Sánchez
authors.forename: Mercedes
authors.initials: M
authors.lastname: Hernández
authors.forename: Teresita
authors.initials: T
authors.lastname: Sainz
authors.forename: Eugene
authors.initials: E
authors.lastname: Bratoeff
mesh_terms: D000818:Animals; D001483:Base Sequence; D051607:CDP-Diacylglycerol-Inositol 3-Phosphatidyltransferase / Q000235:genetics; D006224:Cricetinae; D017931:DNA Primers / Q000235:genetics; D013186:Farnesyl-Diphosphate Farnesyltransferase / Q000235:genetics; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D005992:Glycerol-3-Phosphate O-Acyltransferase / Q000235:genetics; D006903:Hydroxymethylglutaryl CoA Reductases / Q000235:genetics; D016912:Levonorgestrel / Q000494:pharmacology; D050356:Lipid Metabolism / Q000187:drug effects / Q000235:genetics; D008647:Mesocricetus; D011374:Progesterone / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D012627:Sebaceous Glands / Q000187:drug effects* / Q000378:metabolism*; D012867:Skin / Q000187:drug effects / Q000378:metabolism; D013256:Steroids / Q000737:chemistry / Q000378:metabolism / Q000494:pharmacology*; D013739:Testosterone / Q000494:pharmacology
chemical_list: D017931:DNA Primers; D012333:RNA, Messenger; D011980:Receptors, Progesterone; D013256:Steroids; D013739:Testosterone; D011374:Progesterone; D016912:Levonorgestrel; D006903:Hydroxymethylglutaryl CoA Reductases; D005992:Glycerol-3-Phosphate O-Acyltransferase; D013186:Farnesyl-Diphosphate Farnesyltransferase; D051607:CDP-Diacylglycerol-Inositol 3-Phosphatidyltransferase