Neural injections of Bromodeoxyuridine (BrdU) were applied to males of both groups to test for neurogenesis . Analysis showed that testosterone and dihydrotestosterone regulated adult hippocampal neurogenesis (AHN). Adult hippocampal neurogenesis was regulated through the androgen receptor in the wild-type male rats, but not in the TMF male rats. To further test the role of activated androgen receptors on AHN, flutamide , an antiandrogen drug that competes with testosterone and dihydrotestosterone for androgen receptors , and dihydrotestosterone were administered to normal male rats. Dihydrotestosterone increased the number of BrdU cells, while flutamide inhibited these cells.
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Sex hormone-binding globulin (SHBG) is a glycoprotein responsible for the transport and biologic availability of sex steroid hormones, primarily testosterone and estradiol. SHBG has been associated with chronic diseases including type 2 diabetes (T2D) and with hormone-sensitive cancers such as breast and prostate cancer. We performed a genome-wide association study (GWAS) meta-analysis of 21,791 individuals from 10 epidemiologic studies and validated these findings in 7,046 individuals in an additional six studies. We identified twelve genomic regions (SNPs) associated with circulating SHBG concentrations. Loci near the identified SNPs included SHBG (rs12150660, , p = × 10(-106)), PRMT6 (rs17496332, , p = × 10(-11)), GCKR (rs780093, , p = × 10(-16)), ZBTB10 (rs440837, , p = × 10(-09)), JMJD1C (rs7910927, , p = × 10(-35)), SLCO1B1 (rs4149056, , p = × 10(-08)), NR2F2 (rs8023580, , p = × 10(-12)), ZNF652 (rs2411984, , p = × 10(-14)), TDGF3 (rs1573036, , p = × 10(-14)), LHCGR (rs10454142, , p = × 10(-07)), BAIAP2L1 (rs3779195, , p = × 10(-08)), and UGT2B15 (rs293428, , p = × 10(-06)). These genes encompass multiple biologic pathways, including hepatic function, lipid metabolism, carbohydrate metabolism and T2D, androgen and estrogen receptor function, epigenetic effects, and the biology of sex steroid hormone-responsive cancers including breast and prostate cancer. We found evidence of sex-differentiated genetic influences on SHBG. In a sex-specific GWAS, the loci -UGT2B15 was significant in men only (men p = × 10(-08), women p = , heterogeneity p = ). Additionally, three loci showed strong sex-differentiated effects: -SHBG and -TDGF3 were stronger in men, whereas -ZBTB10 was stronger in women. Conditional analyses identified additional signals at the SHBG gene that together almost double the proportion of variance explained at the locus. Using an independent study of 1,129 individuals, all SNPs identified in the overall or sex-differentiated or conditional analyses explained ~% and ~% of the genetic variation of SHBG concentrations in men and women, respectively. The evidence for sex-differentiated effects and allelic heterogeneity highlight the importance of considering these features when estimating complex trait variance.