https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12899 Wed 11 Apr 2018 15:23:55 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9606 Sat 24 Mar 2018 08:39:39 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13283 Sat 24 Mar 2018 08:15:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21445 Sat 24 Mar 2018 08:05:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16923 Sat 24 Mar 2018 08:00:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21764 –1) from 0–72 h postfertilization (hpf), a developmental window when steroidogenesis is unregulated by pituitary influence, resulted in the up-regulation of cyp11a, cyp17, and 3β-hsd and the down-regulation of cyp19a. Similar gene expression patterns were observed for embryos exposed to 10 mM cobalt chloride (CoCl₂, a chemical inducer of hypoxia-inducible factor 1, HIF-1), suggesting a regulatory role of HIF-1 in steroidogenesis. Testosterone (T) and estradiol (E2) concentrations in hypoxic embryos were greater and lesser, respectively, relative to the normoxic control, thus leading to an increased T/E2 ratio. Expression of the leptin-a gene (zlep-a) was up-regulated upon both hypoxia and CoCl₂ treatments. Functional assays suggested that under hypoxia, elevated zlep-a expression might activate cyp11a and 3β-hsd and inhibit cyp19a. Overall, this study indicates that hypoxia, possibly via HIF-1-induced leptin expression, modulates sex steroid synthesis by acting directly on steroidogenic gene expression.]]> Sat 24 Mar 2018 07:53:07 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19996 Sat 24 Mar 2018 07:50:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25155 Sat 24 Mar 2018 07:14:30 AEDT ]]>