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J. A. Jonassen, S. P. Baker, and A. S. McNeilly


Hyperprolactinaemia disrupts fertility in many species, perhaps by inhibiting ovarian follicular steroidogenesis. The present studies measured oestradiol and progesterone secretion from isolated follicles from rats rendered hyperprolactinaemic in one of two ways. Sustained hyperprolactinaemia was induced by transplantation of two donor pituitary grafts under the renal capsule of adult female rats; grafts remained in place for 3 months. Transient hyperprolactinaemia was induced by pseudopregnancy initiated by cervical stimulation. Small antral follicles were isolated from both groups of rats 8–10 days after the previous vaginal oestrous smear and also from a control group of dioestrous female rats. Follicles were incubated for 3 h in the presence or absence of human chorionic gonadotrophin (hCG) or testosterone. Basal and hCG-stimulated oestradiol production were each reduced in follicles from both hyperprolactinaemic groups, relative to follicles from dioestrous control rats. In contrast, in the presence of testosterone, all groups of follicles produced comparable amounts of oestradiol. hCG stimulated comparable progesterone production by follicles from all three treatment groups. Testosterone elicited smaller increases in progesterone accumulation by follicles from all in-vivo groups. Reduced basal and gonadotrophin-stimulated, but not androgen-stimulated, oestradiol accumulation suggests that androgen production rather than aromatase activity in small antral follicles may be impaired by long-term hyperprolactinaemia.

Journal of Endocrinology (1991) 129, 357–362

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R I G Holt, A J Baker, J S Jones, P A Crossey, N M Stone, V R Preedy, and J P Miell


Hepatic gene expression and circulating levels of IGF-binding proteins (IGFBP)-1 to -4 were examined in two rat models of liver disease employing acute hepatitis or chronic structural damage.

The study comprised four groups: group 1 (n=6) was injected intraperitoneally with saline and food was available ad libitum (AL), group 2 (n=6) underwent bile duct ligation (BDL), group 3 (n=6) was injected with 400 mg galactosamine (GAL), group 4 (n=6) was sham-operated and pair-fed to group 2 (PF). All were killed by decapitation at day 7.

Serum IGF-I, by RIA, was significantly (P<0·05) lower in the BDL group (458 ± 37 μg/l) and PF group (451 ±51 μg/l) compared with the AL group (643 ± 77 μg/l) and GAL group (720 ± 67 μg/l). Immunoblotting showed raised IGFBP-2 levels in all groups compared with AL (BDL, 167 ± 14% of AL; GAL, 173 ± 13%; PF, 149 ± 9%). IGFBP-3 was decreased in the GAL (56 ± 11%) and PF groups (66 ± 5%) but increased in the BDL group (154 ± 29%). IGFBP-4 was decreased in the GAL (76 ± 11%) and PF groups (47 ± 5%) but unchanged in the BDL group (90 ± 10%).

By Northern analysis, IGFBP-1 mRNA expression was increased in the GAL (321 ± 51%) and PF groups (263 ± 12%) but reduced in the BDL group (68 ± 8%). IGFBP-2 expression increased in all groups (PF, 836 ± 19%; BDL, 683 ± 121%; GAL, 372 ± 68%) and was highest in the BDL and PF groups. IGFBP-3 expression was reduced in all groups (BDL, 57 ± 16%; GAL, 52 ± 12% PF, 51 ± 13%). IGFBP-4 expression was reduced in the GAL (30 ± 4%) and PF (28 ± 5%) groups but unchanged in the BDL group (76 ± 9%).

Marked changes in gene expression of IGFBPs occurred in both models of liver disease, together with serum changes, which were different from each other and from malnutrition alone.

Journal of Endocrinology (1996) 149, 465–472