title: Androgen, estrogen, and progesterone receptor gene regulation during diabetic erectile dysfunction and insulin treatment.
abstract: OBJECTIVE
  To determine whether altered levels of sex hormone receptor genes (androgen, estrogen, and progesterone receptors) are involved in the etiology of diabetes-related erectile dysfunction. Insulin treatment can restore erectile function through modulation of sex hormone receptor genes.
  
  
  METHODS
  Diabetes was induced in rats (n = 40) by intraperitoneal injection of streptozotocin. The diabetic rats were divided into two groups: untreated rats (n = 20) and rats treated daily with 10 U subcutaneous human recombinant insulin (n = 20). Control nondiabetic rats (n = 20) were given only vehicle. Erectile function was analyzed by measurement of intracavernous pressure. Gene and protein expression of sex hormone receptors were analyzed by reverse transcriptase-polymerase chain reaction and immunohistochemistry, respectively.
  
  
  RESULTS
  The mean intracavernous pressure was significantly decreased in the diabetic rats compared with the controls and was restored to normal after insulin treatment. In the diabetic rat crura, mRNA and protein expression for estrogen receptor-beta and progesterone receptor were significantly lower than in the control crura, and the expression profile of androgen receptor and estrogen receptor-beta did not change. Insulin treatment restored estrogen receptor-beta and progesterone receptor mRNA and protein expression. Insulin treatment significantly increased the expression of mRNA and protein for androgen receptor and estrogen receptor-alpha in diabetic rats compared with control rats.
  
  
  CONCLUSIONS
  This is the first study to demonstrate that insulin treatment may restore erectile function through restoration of sex hormone receptor gene and protein expression in the diabetic rat crura.
authors.affiliation: Department of Urology, Veterans Affairs Medical Center and University of California, San Francisco, School of Medicine, San Francisco, California 94121, USA.
authors.forename: Masato
authors.initials: M
authors.lastname: Shirai
authors.forename: Masaki
authors.initials: M
authors.lastname: Yamanaka
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Shiina
authors.forename: Mikio
authors.initials: M
authors.lastname: Igawa
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Ogishima
authors.forename: Makoto
authors.initials: M
authors.lastname: Fujime
authors.forename: Nobusiha
authors.initials: N
authors.lastname: Ishii
authors.forename: Akihiko
authors.initials: A
authors.lastname: Okuyama
authors.forename: Tom F
authors.initials: TF
authors.lastname: Lue
authors.forename: Rajvir
authors.initials: R
authors.lastname: Dahiya
mesh_terms: D000818:Animals; D048909:Diabetes Complications / Q000188:drug therapy* / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000378:metabolism; D007172:Erectile Dysfunction / Q000188:drug therapy* / Q000209:etiology* / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects*; D007328:Insulin / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D011944:Receptors, Androgen / Q000235:genetics / Q000378:metabolism; D011960:Receptors, Estrogen / Q000235:genetics / Q000378:metabolism; D011980:Receptors, Progesterone / Q000235:genetics / Q000378:metabolism; D011987:Receptors, Steroid / Q000235:genetics / Q000378:metabolism*
chemical_list: D007328:Insulin; D011944:Receptors, Androgen; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D011987:Receptors, Steroid