title: 17α-Estradiol and genistein inhibit high fat diet induced prostate gene expression and prostate growth in the rat.
abstract: OBJECTIVE
  High dietary fat and low phytoestrogen intake are associated with prostate cancer development and progression. Our previous study showed that exposure to a high fat diet significantly increased prostate 5α-reductase-2 mRNA and prostate growth in the rat. In the current experiments we determined the effects of genistein and 17α-estradiol on the modulation of dietary fat induced prostate 5α-reductase-2 and insulin-like growth factor-1 gene expression, and prostate growth.
  
  
  METHODS
  At weaning male ACI/Seg rats (Harlan® Sprague-Dawley®) were fed a low or a high fat diet, with or without genistein or 17α-estradiol for 2, 4 or 10 weeks. The prostate was dissected and weighed. We determined the levels of prostate 5α-reductase-2 mRNA, insulin-like growth factor-1 mRNA, dihydrotestosterone, and plasma insulin-like growth factor-1, dihydrotestosterone and testosterone.
  
  
  RESULTS
  Two-week exposure to a high fat diet significantly increased prostate insulin-like growth factor-1 mRNA without significant changes in plasma insulin-like growth factor-1, which was blocked by genistein and 17α-estradiol. Genistein but not 17α-estradiol also inhibited prostate 5α-reductase-2 mRNA and intraprostatic dihydrotestosterone induced by the high fat diet at 2 weeks. Genistein and 17α-estradiol completely blocked high fat diet induced prostate growth at 10 weeks of dietary treatment. However, neither genistein nor 17α-estradiol had any significant effect when co-administered with the low fat diet.
  
  
  CONCLUSIONS
  Results indicate that genistein and 17α-estradiol can inhibit dietary fat induced changes in prostate 5α-reductase-2 and insulin-like growth factor-1 gene expression, and prostate growth in the rat. This may be beneficial to prevent dietary fat associated prostate diseases such as prostate cancer.
authors.affiliation: Department of Medicine/Endocrinology, Weill Cornell Medical College, New York, New York 10065, USA.
authors.forename: Li-Qun
authors.initials: LQ
authors.lastname: Cai
authors.forename: Jingjing
authors.initials: J
authors.lastname: Cai
authors.forename: Wendy
authors.initials: W
authors.lastname: Wu
authors.forename: Yuan-Shan
authors.initials: YS
authors.lastname: Zhu
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D042944:Cholestenone 5 alpha-Reductase / Q000235:genetics* / Q000378:metabolism; D004041:Dietary Fats / Q000494:pharmacology*; D013196:Dihydrotestosterone / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects; D019833:Genistein / Q000494:pharmacology*; D007334:Insulin-Like Growth Factor I / Q000235:genetics* / Q000378:metabolism; D008297:Male; D048789:Phytoestrogens / Q000494:pharmacology*; D011467:Prostate / Q000187:drug effects / Q000254:growth & development*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013739:Testosterone / Q000378:metabolism
chemical_list: D004041:Dietary Fats; D048789:Phytoestrogens; D012333:RNA, Messenger; D013196:Dihydrotestosterone; D013739:Testosterone; D004958:Estradiol; D007334:Insulin-Like Growth Factor I; D019833:Genistein; D042944:Cholestenone 5 alpha-Reductase