Numerous studies have suggested that ovarian hormones are able to modulate insulin sensitivity, but their exact role remains unclear. We have investigated whether different doses of 17beta-oestradiol mediate changes in insulin sensitivity and if these changes could be related to modifications of insulin receptor substrate-1 (IRS-1). Female rats were ovariectomized and later separated into three groups: untreated; treated with a dose of 17beta-oestradiol sufficient to reproduce gestational plasma concentrations of 17beta-oestradiol (group E); and treated with a dose 100 times greater than that given to group E (group E2). A euglycaemic-hyperinsulinaemic clamp was used to measure insulin sensitivity. Changes in IRS-1 were analysed by Western blotting and RT-PCR assays. In group E we found a decrease in insulin sensitivity between days 11 and 16 of treatment as in late gestation, whereas in the untreated group and group E2, development of insulin resistance was observed throughout the treatment. In contrast, whereas in group E2 insulin resistance throughout the hormonal treatment was related to diminished expression and phosphorylation of IRS-1, in group E the decrease in insulin sensitivity between days 11 and 16 of treatment was not related to a decrease in IRS-1 expression. Our results suggest that the effects of oestradiol on insulin sensitivity were dose-dependent and that the insulin resistance associated with a high dose of 17beta-oestradiol was related to downregulation of IRS-1 expression.
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C Gonzalez, A Alonso, F Diaz, and AM Patterson
A. E. CASTRO, A. ALONSO, and R. E. MANCINI
SUMMARY
Rabbit antisera to ovine follicle-stimulating (FSH) and luteinizing (LH) hormones were used in the indirect fluorescent antibody technique on sections of rat testis to detect intravenously injected FSH or LH. A direct method using ferritin-labelled rabbit anti-LH globulins was also performed on sections of testis from LH-injected rats. Follicle-stimulating hormone was localized in the Sertoli cells while LH appeared mainly in the interstitial and peritubular cells. These results agree with previous observations on the cellular distribution of both gonadotrophins in the rat testis.
C Gonzalez, A Alonso, N Alvarez, F Diaz, M Martinez, S Fernandez, and AM Patterson
The mechanism for the development of insulin resistance in normal pregnancy is complex and is associated with serum levels of both progesterone and 17beta-estradiol. However, it remains unclear whether estrogens alone or progestins alone can cause insulin resistance, or whether it is a combination of both which produces this effect. We attempted to determine the role played by progesterone and/or 17beta-estradiol on the phenomena of sensitivity to insulin action that take place during pregnancy in the rat. Ovariectomized rats were treated with different doses of progesterone and/or 17beta-estradiol in order to simulate the plasma levels in normal pregnant rats. A euglycemic/hyperinsulinemic clamp was used to measure insulin sensitivity. At days 6 and 11, vehicle (V)- and progesterone (P)-treated groups were more insulin resistant than 17beta-estradiol (E)- and 17beta-estradiol+progesterone (EP)-treated groups. Nevertheless, at day 16, the V, EP and E groups were more resistant to insulin action than the P group. On the other hand, the V, EP and E groups were more insulin resistant at day 16 than at day 6, whereas the P group was more insulin resistant at day 6 than at day 16. Our results seem to suggest that the absence of female steroid hormones gives rise to a decreased insulin sensitivity. The rise in insulin sensitivity during early pregnancy, when the plasma concentrations of 17beta-estradiol and progesterone are low, could be due to 17beta-estradiol. However, during late pregnancy when the plasma concentrations of 17beta-estradiol and progesterone are high, the role of 17beta-estradiol could be to antagonize the effect of progesterone, diminishing insulin sensitivity.
G. A. Jahn, G. A. Machiavelli, L. E. Kalbermann, I. Szijan, G. E. Alonso, and J. A. Burdman
The effect of daily injections of sulpiride was compared with that of a single injection of the drug in male rats which had been treated with oestradiol diundecenoate for various periods of time. We studied the effect of the different treatments on weight of the pituitary gland, concentration of prolactin and incorporation of [3H]thymidine into DNA in the pituitary gland and on serum levels of prolactin. Administration of the oestrogen produced a marked increase in the synthesis of DNA at day 7. The stimulation diminished at day 21 and was not significant at day 45. The maximum increase in the concentration of prolactin in serum and pituitary glands was observed during the first 7 days (approximately 400 and 150% respectively) and in the weight of the anterior pituitary gland after 21 days of treatment (approximately 107%).
A single injection of sulpiride markedly stimulated the release of prolactin and the synthesis of DNA at day 7. Both these effects diminished at day 21 and disappeared by day 45. Daily injections of sulpiride also produced similar changes in the release of prolactin and in the replication of DNA. The growth of the anterior pituitary gland was greater in this group than in the rats which had been treated with oestradiol diundecenoate only. After the end of treatment with oestrogen and sulpiride the pituitary weight and the concentration of prolactin in the anterior pituitary gland diminished together with levels of prolactin and oestrogen in serum. There was a good correlation between weight of the gland and serum levels of prolactin. The results further support the idea of a mechanism which controls the proliferation of lactotrophs in which the release of the hormone is accompanied by an increase in pituitary DNA synthesis.
J E Sánchez-Criado, G Hernandez, C Bellido, D Gonzalez, M Tébar, M A Diaz-Cruz, and R Alonso
Abstract
The antiprogesterone RU486 injected on the morning of pro-oestrus blunts the preovulatory secretion of LH and FSH and abolishes the secondary secretion of FSH during oestrus without affecting ovulation in the rat. To ascertain whether the secretion of LHRH is involved in these effects, we studied the effects of RU486 (4 mg/0·2 ml oil), given s.c. at 0800 h on pro-oestrus, on LHRH secretion into the pituitary stalk blood vessels and on peripheral plasma concentrations of LH and FSH at 1800 h on pro-oestrus and 0200 h on oestrus. Furthermore, we determined the effects of an s.c. injection of 1 mg of an LHRH antagonist (LHRH-A; ORG30276) at 2000 h on pro-oestrus and those of an i.p. injection of 100 ng LHRH (Peninsula 7201) at 0100 h on oestrus on serum concentrations of LH, FSH and oestradiol at 0200 h on oestrus in oil- and RU486-treated rats.
RU486 decreased LHRH secretion at 1800 h on prooestrus while this was increased at 0200 h on oestrus. While the reduction of preovulatory LHRH secretion in RU486-treated rats coincided with a reduction in both LH and FSH surges during the evening of pro-oestrus, the increased LHRH secretion during the early hours of oestrus was only accompanied by an increased concentration of LH. An injection of LHRH stimulated, while that of LHRH-A inhibited serum concentrations of LH at 0200 h on oestrus in both oil- and RU486-treated rats. An injection of LHRH-A had no effect on FSH concentration at 0200 h on oestrus in either oil- or RU486-treated rats. On the contrary, exogenous LHRH increased FSH concentration at 0200 h on oestrus only in oil-treated rats.
The results indicate that, in the rat, progesterone secretion during the afternoon and evening of pro-oestrus enhances preovulatory LHRH and suppresses LHRH release during early oestrus into the pituitary stalk blood vessels on the afternoon of pro-oestrus and during early oestrus respectively. While the secretion of LH during early oestrus is blunted by progesterone and entirely coupled to LHRH secretion, the secondary secretion of FSH during oestrus is not dependent on endogenous LHRH and at the same time is completely dependent on the actions (direct and/or indirect) of progesterone.
Journal of Endocrinology (1994) 141, 7–14
María E Trujillo-Ortega, Daniel Mota-Rojas, Rafael Hernández-González, Elvia Yadira Velázquez-Armenta, Alejandro A Nava-Ocampo, Ramiro Ramírez-Necoechea, Marcelino Becerril-Herrera, and María Alonso-Spilsbury
This study aimed to investigate whether the administration of recombinant porcine somatotropin (rpST) late in gestation is associated with increased rates of obstetric and neonatal complications in primiparous sows. From days 80 to 114 of gestational age, 20 primiparous sows were randomly assigned to receive an intramuscular injection of either saline or 6 mg rpST/day. Throughout pregnancy, sows were fed 2.5 to 3 kg/day of a corn-soybean diet (14 MJ ME/kg). Of 111 piglets born to control sows and 109 piglets born to treated sows, 8.1% and 17.4% piglets respectively died intrapartum (P=0.04). Glucose blood levels in sows and live-born piglets in the rpST-treated group were significantly higher than in their corresponding controls. Birth weight of live-born piglets in the treated group was 1.4 ± 0.1 kg versus 1.3 ± 0.1 kg in the control group (P<0.0001). Birth weight of piglets born dead was also higher in the former than in the latter group (P<0.0001). No evidence of teratogenicity was observed in either of the groups. In conclusion, rpST administration in late pregnancy to primparous sows increased the rate of neonatal deaths and was associated with higher blood glucose levels in both sows and piglets.
