Search PubMed⌕ Search

Biomedical subjects

F Labrie

Publications and source records attributed to F Labrie.

At least 613 records · Page 34Linked to original sources
PubMed1977

Stimulated release of hypothalamic growth hormone-releasing activity by morphine and pentobarbital.

Two minutes after the intravenous administration of 1 ml of sheep somatostatin antiserum in the rat, plasma growth hormone (GH) levels had reached a maximal 10-15-fold increase which remained approximately constant up to 90 min. The injection of sodium pentobarbital (2 mg/100 g body wt) led to a rapid and transient rise of plasma GH levels of similar magnitude (10-fold) reached 20 to 40 min after injection of the narcotic. The important finding is, however, that the combined administration of somatostatin antiserum and pentobarbital or morphine led to an almost exact additive effect on the plasma GH concentrations. These data, beside providing additional evidence for the existence of GH-releasing activity (GH-RH), indicate that morphine and pentobarbital stimulate GH secretion through increased release of GH-RH.

Animals↗
PubMed1977

High inhibitory activity of R 5020, a pure progestin, at the hypothalamic-adenohypophyseal level on gonadotropin secretion.

Synthetic "progestins" currently used in the contraceptive pill inhibited the luteinizing hormone (LH) responsiveness to LH-releasing hormone in cells in culture in a way undistinguishable from that of androgens. Moreover, they competed for binding of the 3H-labeled androgen R 1881 to the rat prostate androgen receptor and stimulated seminal vesicle and prostate weight in castrated rats. R 5020, a pure progestin, was without effect on the above-mentioned parameters. However, a complete inhibition of the LH surge measured in the afternoon of expected proestrus was obtained at a dose of R 5020 similar to that of D-norgestrel. The synthetic progestin was also found to inhibit ovulation and to delay vaginal cornification. The present data show that the synthetic "progestins" commonly used in the pill possess intrinsic androgenic activity which could well be responsible, to an unknown extent, for their effectiveness as contraceptive agents. R 5020, a synthetic progestin devoid of androgenic activity, is at least as potent as the most potent 19-nortestosterone derivative, D-norgestrel, in inhibiting gonadotropin secretion and other parameters of the estrous cycle in the rat. The availability of a pure progestin devoid of androgenic activity but highly effective as an inhibitor of gonadotropin secretion could be of great interest for the development of an improved contraceptive.

Animals↗
PubMed1977

Beta-endorphin: stimulation of growth hormone release in vivo.

Two micrograms of beta-endorphin (beta-lipotropin61-91) injected intraventricularly in rats that had been treated with antiserum against somatostatin led to a 6- and 10-fold stimulation of the concentration of plasma growth hormone (somatotropin) measured 10 and 20 min after injection of the peptide, whereas 400 mug of methionine-enkephalin led to a 4- to 6-fold increase of levels of plasma growth hormone at 10 min with a rapid return to basal levels at later time intervals. At doses of 5 and 25 mug, beta-endorphin led to a 20- to 30-fold stimulation of levels of plasma growth hormone, the maximal effect being measured between 20 and 30 min after injection. These data suggest the possible role of the endogenous opiate-like peptides in the control of growth hormone secretion.

Animals↗
PubMed1977

Potent inhibitory effect of a new antiestrogen (RU 16117) on the growth of 7,12-dimethylbenz[a]anthracene-induced rat mammary tumors.

At the daily dose of 24 mug for a period of 4 weeks, RU 16117 (11alpha-methoxyethinyl estradiol), a new antiestrogen, led to 65% reduction of the number of already established dimethylbenz[a]anthracene (DMBA)-induced mammary tumors in female Sprague-Dawley rats. Not only the tumor number but also the tumor size was reduced by RU 16117 in a manner similar to that seen after ovariectomy. The absence of an inhibitory effect of doses of 0.1 to 12.5 mug 17beta-estradiol (E2) per day, a dose-range which covers the low estrogenic activity of the RU 16117 doses used, suggested that the inhibitory effect of RU 16117 was not due to its estrogenic activity. Decreased levels of receptors for E2, progesterone, and prolactin were found in the tumors remaining after ovariectomy; treatment with the dose of RU 16117 sufficient to inhibit tumor growth (24 mug) had a similar inhibitory effect on the levels of E2 and prolactin receptors. These data suggested that a reduction of hormone receptor levels in the tumor tissue could be a mechanism by which RU 16117 acts as a potent inhibitor of the growth of DMBA-induced mammary carcinoma.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1977

Purification of plasma membrane fractions from the bovine pars intermedia and neurohypophyseal lobe and properties of associated adenylate cyclase.

A procedure for the isolation of plasma-membrane-enriched fractions from bovine 'pars intermedia' and neurohypophysis is described. Various fractions are isolated by differential centrifugation and discontinuous sucrose density gradients. The plasma-membrane-enriched fractions have a density in sucrose of 1.14 and 1.16 and the yields are 1.8 mg and 1.5 mg per gram of tissue for the pars intermedia and neural lobe, respectively. The fractions are characterized by electron microscopy and enzymatic assays. The plasma membrane fractions are mainly vesicular in nature and are free of nuclei, mitochondria, and microsomes when examined by electron microscopy. 5'-Nucleotidase (EC 3.1.3.5) and Mg2+-(Na+ + K+)-ATPase (EC 3.6.1.3) activities are concentrated in the plasma-membrane-enriched fraction. Also, adenylate cyclase (EC 4.61.1) shows a 5 to 10-fold purification in the isolated membrane fraction. NaF (10mM) gives a two to three-fold stimulation of enzymatic activity in all fractions studied The yields of adenylate cyclase, 5'-nucleotidase, and Mg2+-(Na+ +K+)-ATPase are about 6% in the membrane fraction.

Adenosine Triphosphatases↗
PubMed1977

Sensitizing effect of treatment with estrogens on TSH response to TRH in male rats.

Daily administration of estradiol benzoate (10 microgram/100 g body wt) to intact male rats led to a twofold increase of the plasma TSH (thyroid-stimulating hormone) response to thyrotropin-releasing hormone (TRH) after 4 and 7 days of treatment whereas the basal plasma TSH level was not affected. The basal plasma PRL concentration and the PRL response to TRH were both markedly increased by estrogen treatment. The TSH pituitary content remained unchanged, whereas the PRL pituitary content increased in parallel with the effect on PRL secretion. Treatment with estrogens for 1 wk sensitized the TSH secretory response to low doses of TRH (10 ng), whereas no significant effect on the response was found at high doses of the neurohormone. The present data show that the stimulatory effect of estrogens on the TSH response to TRH is due to true sensitization of the thyrotrophs to the action of the neurohormone, whereas that on prolactin secretion can result partly from increased pituitary prolactin content.

Animals↗
PubMed1977

Immunohistochemical localization of beta-lipotropic hormone in the pituitary gland.

Identification of the beta-lipotropic hormone (beta-LPH)-producing cells in several species, including man, was performed with the technique involving use of the unlabeled antibody and peroxidase-antiperoxidase complex. Serial paraffin and ultrathin sections were treated for detection of both beta-LPH and ACTH at the light and electron microscopic levels. It was clearly shown that beta-LPH could be found only in the corticotropic cells located in the pars intermedia and pars distalis of all species studied. At the electron microscope level, it could be established that beta-LPH is contained in all the secretory granules of positive cells. These results suggest that beta-LPH is stored in the same secretory granules as ACTH and that both hormones are released together during granule extrusion.

Animals↗
PubMed1977

Modulation of pituitary thyrotropin releasing hormone receptor levels by estrogens and thyroid hormones.

The effect of estradiol and thyroid hormone treatment on pituitary TRH binding and TSH and PRL responses to the neurohormone was studied. A significant increase in the number of pituitary TRH binding sites was observed between 2 and 4 days after daily administration of estradiol benzoate with a plateau at 300% of control being reached at 7 days. Plasma PRL levels showed a similar early pattern of response. In animals rendered hypothyroid by a 2-month treatment with propylthiouracil or 1 month after surgical thyroidectomy, the level of pituitary TRH receptors was increased approximately 2-fold, this elevation being completely reversed by treatment with thyroid hormone. Estradiol-17beta administered with L-thyroxine partially reversed the inhibitory effect of thyroid hormone on TRH receptor levels in hypothyroid animals. The antagonism between estrogens and thyroid hormone is also apparent on the TSH response to TRH since estrogen administration can reverse the marked inhibition by thyroxine of the TSH response to TRH either partially or completely in intact and hypothyroid animals, respectively. The PRL response to TRH is 55 and 40% inhibited in hypothyroid and intact rats, respectively, by thyroid hormone when combined with estrogen treatment. The present data clearly show that estrogens and thyroid hormones can affect TSH and PRL secretion, the effect of estrogens being predominantly on PRL secretion while thyroid hormone affects mainly TSH. The close correlation observed between the level of TRH receptors and PRL and TSH responses to TRH suggests that estrogens and, to a lesser extent, thyroid hormones, exert their action by modulation of the level of receptors for the neurohormone in both thyrotrophs and mammotrophs.

Animals↗
PubMed1977

Changes of pituitary thyrotropin releasing hormone (TRH) receptor level and prolactin response to TRH during the rat estrous cycle.

The plasma PRL and TSH responses to TRH injected iv at different stages of the estrous cycle in normal rats under Surital anesthesia were maximal during the afternoon of proestrus and morning of estrus and lowest on diestrus I. As calculated from the areas under the plasma response curves, a 10-fold difference was found between the maximal and minimal PRL responses while a 2-fold difference was measured for TSH. The plasma PRL and TSH responses to TRH showed a correlation with the binding of [3H]TRH to anterior pituitary gland, a 3-fold difference being observed between the minimal binding measured on the morning of diestrus II and the maximal value found on the evening of proestrus. Contrary to findings with LHRH and LH, repeated injections of a small dose (10 ng) of TRH in the afternoon of proestrus abolished PRL and TSH responses to subsequent injection of the neurohormone.

Animals↗
PubMed1977

Potent inhibitory activity of [D-Leu6, Des-Gly-NH2(10)]LHRH ethylamide on LH/hCG and PRL testicular receptor levels in the rat.

Injection of male rats with 40-200 ng of [D-Leu6, des-Gly-NH2(10)]LHRH ethylamide for 7 days caused a maximal 80% reduction of testicular LH/hCG receptor level with one injection per day being as efficient as 3 daily injections. A similar inhibitory effect was observed on testicular PRL receptors. Testis and seminal vesicle weight as well as plasma testosterone levels were also significantly reduced by this treatment. These data indicate that a LHRH agonist, when given at a relatively low dose, is capable of reducing testicular LH/hCG and PRL receptor levels as well as testicular function, the effect being probably mediated by increased endogenous gonadotropin secretion.

Animals↗