title: Exendin-4 shows no effects on the prostatic index in high-fat-diet-fed rat with benign prostatic hyperplasia by improving insulin resistance.
abstract: Benign prostatic hyperplasia (BPH) is a prevalent disease globally, and accumulating evidence has indicated an association between BPH, insulin resistance (IR) and diabetes. Exendin-4 is widely used in clinics, which could enhance the proliferation of pancreatic β cells. The ability of exendin-4 to promote tumorigenesis has been of concern, and whether exendin-4 would enhance the propagation of BPH is not fully understood. We aimed to determine whether glucagon-like peptide-1 receptors (GLP-1Rs) were expressed in rat prostate and to determine the effect of exendin-4 on prostate of BPH. Male Wistar rats were used and assigned to six groups: normal diet (ND), high-fat diet (HFD), HFD + exendin-4, HFD + BPH, HFD + BPH + exendin-4 and HFD + BPH + rosiglitazone group. After castration, steroids were injected subcutaneously for 4 weeks to induce BPH. Rats were kept on high-fat diet to induce IR. Treatment groups were treated with exendin-4 and rosiglitazone. Prostatic index and HOMA-IR index were used to evaluate the prostatic hyperplasia status and the degree of IR respectively. The expression of GLP-1R was indicated not only by immunohistochemistry, but also by Western blot analysis. The expression of GLP-1R was significantly higher, and HOMA-IR index and body weight significantly decreased after administration of exendin-4. However, no significant differences in the prostatic index were observed between exendin-4 treatment groups and non-exendin-4 treatment groups. Prostatic index was not influenced by exendin-4 maybe by improving IR and weight loss.
authors.affiliation: Department of Endocrinology, The First Clinical Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
authors.forename: J-X
authors.initials: JX
authors.lastname: Zheng
authors.forename: Y-C
authors.initials: YC
authors.lastname: Xiao
authors.forename: Y-R
authors.initials: YR
authors.lastname: Hu
authors.forename: M
authors.initials: M
authors.lastname: Hao
authors.forename: H-Y
authors.initials: HY
authors.lastname: Kuang
mesh_terms: D000818:Animals; D001835:Body Weight / Q000187:drug effects; D059305:Diet, High-Fat; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D000077270:Exenatide; D000067757:Glucagon-Like Peptide-1 Receptor; D007333:Insulin Resistance; D008297:Male; D010455:Peptides / Q000494:pharmacology* / Q000627:therapeutic use; D011467:Prostate / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D011470:Prostatic Hyperplasia / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D018027:Receptors, Glucagon / Q000378:metabolism; D000077154:Rosiglitazone; D012720:Severity of Illness Index; D045162:Thiazolidinediones / Q000494:pharmacology; D014688:Venoms / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: C000593835:Glp1r protein, rat; D000067757:Glucagon-Like Peptide-1 Receptor; D010455:Peptides; D018027:Receptors, Glucagon; D045162:Thiazolidinediones; D014688:Venoms; D000077154:Rosiglitazone; D000077270:Exenatide
keywords: Benign prostatic hyperplasia; exendin-4; glucagon-like peptide-1; glucagon-like peptide-1 receptor; insulin resistance