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At least 343 records · Page 19Linked to original sources
PubMed1992

Control of thyroid secretion: effects of stimulators of protein kinase C, thyrotropin, and calcium mobilization on secretion of iodinated compounds from sheep thyroid cells.

We have compared and contrasted the abilities of TSH and agents capable of discretely activating the cAMP-dependent protein kinase, protein kinase C, or calcium mobilization to influence the secretion of iodinated compounds from cells prelabeled with iodide and blocked from further organification with methimazole. We found that calcium mobilization induced by A23187, protein kinase C activation induced by 12-O-tetradecanoyl phorbol 13-acetate (TPA) and TSH all stimulated the secretion of iodinated compounds. The effects of TSH were mimicked by forskolin and those of TPA by a synthetic diacylglycerol, sn-1,2-dioctanoylglycerol. The effects of TPA were partially inhibited by staurosporine whereas those of TSH were not. Epidermal growth factor and norepinephrine were without effect on thyroid secretion. The effects of A23187 and TPA were synergistic. The effects of TSH and TPA were not and the increased secretion induced by either agent was partially prevented by the combination. Preincubation of cells with TSH desensitized the cells to further stimulation by TSH but the stimulatory effects of TPA were unaffected. Exposure of cells to medium without calcium also induced loss of iodinated compounds which was partially prevented by TSH or forskolin but not TPA. TSH did not stimulate the rapid production of inositol trisphosphate production. We conclude that the mechanisms by which TSH (through stimulation of cAMP) and stimulators of other intracellular pathways exert their effects on secretion of iodocompounds, differ. Activation of protein kinase C and acute production of inositol trisphosphate do not appear to be involved in the mechanism of action of TSH in stimulating thyroid secretion but calcium mobilization is implicated.

Alkaloids↗
PubMed1995

Cyclic adenosine-3',5'-monophosphate stimulates mouse placental lactogen-I (mPL-I) secretion but inhibits mPL-II secretion at midpregnancy.

To determine whether cAMP regulates mouse placental lactogen-I (mPL-I) and mPL-II secretion at midpregnancy in vitro, mouse placental tissue from day 9 of pregnancy was dispersed with collagenase, cells were fractionated on a Percoll gradient, and the purified trophoblast cells were plated in a serum-free medium. The cells were then incubated with various agents that increased the intracellular cAMP level for 5 days. 8-Bromo-cAMP stimulated mPL-I secretion, but inhibited mPL-II secretion in a time- and dose-dependent manner without changing the amount of newly synthesized trichloroacetic acid-precipitable proteins. Cholera toxin and forskolin, which increase intracellular cAMP accumulation, also regulated mPL-I and mPL-II secretion in the same manner. 8-Bromo-cAMP increased the intracellular mPL-I concentration, decreased the intracellular mPL-II concentration, and increased the immunoprecipitable newly synthesized mPL-I concentration in both the medium and cells. 8-Bromo-cAMP increased the expression of mPL-I messenger RNA and decreased the expression of mPL-II messenger RNA. The sequential reverse hemolytic plaque assay and double immunocytochemistry indicated that 8-bromo-cAMP regulates the subpopulation of giant cells containing and releasing mPL. These findings suggest that an increase in intracellular cAMP stimulates mPL-I secretion, but inhibits mPL-II secretion by changing the subpopulation of giant cells containing and releasing mPL.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1985

Adrenocorticotropin-stimulated adrenal androgen secretion in anorexia nervosa: impaired secretion at low weight with normalization after long-term weight recovery.

Adrenal androgen secretion is decreased in patients with anorexia nervosa. To assess the reversibility of the decreased secretion with recovery of body weight, we measured ACTH-stimulated adrenal androgen levels at different stages of recovery. Basal plasma GH and somatomedin-C levels also were measured, because both have been proposed as potential stimuli for adrenal androgen secretion. When studied at low body weight [58 +/- 3% (+/- SEM) ideal BW], women with anorexia nervosa had decreased ACTH-stimulated levels of dehydroepiandrosterone (DHA), DHA sulfate (DHAS), and androstenedione and decreased DHA to cortisol, DHAS to cortisol, and androstenedione to cortisol ratios compared to normal women. Women who had recently completed a refeeding program (within 2-4 weeks, 81 +/- 2% ideal BW) had an increased somatomedin-C level compared to low weight patients, but similar ACTH-stimulated adrenal androgen levels. Long term weight-recovered women (86 +/- 4% ideal BW, recovery for more than 6 months, with resumption of menses), however, had significant increases in ACTH-stimulated DHA and DHAS levels and DHA to cortisol and DHAS to cortisol ratios, and their hormone levels and ratios were not different from those in normal women. GH levels fell during weight recovery, although the values in the three patient groups did not differ significantly. We conclude that the recovery of adrenal androgen secretion while GH levels were falling provides evidence against a direct effect of GH as a stimulus for adrenal androgen secretion. The recovery of somatomedin-C before the recovery of adrenal androgens, however, and the positive correlation between plasma somatomedin-C and the integrated level of plasma DHAS (r = 0.50; P less than 0.02) are consistent with the hypothesis that somatomedin-C is a stimulus for adrenal androgen secretion.

Adrenal Glands↗
PubMed1985

Pulsatile gonadotropin secretion in women with hypothalamic amenorrhea: evidence that reduced frequency of gonadotropin-releasing hormone secretion is the mechanism of persistent anovulation.

Hypothalamic amenorrhea (HA) is a clinical disorder of unknown etiology. The diagnosis is made by exclusion of known abnormalities of pituitary and ovarian function. To determine if abnormalities of GnRH secretion could account for the anovulation and amenorrhea, we measured plasma gonadotropins every 20 min for 10- to 24-h periods in 19 women with HA. Ovarian steroids and gonadotropin responses to an iv bolus dose of GnRH (25 ng/kg) were also measured. The results were compared to those obtained during the early follicular (EF) and late luteal (LL) phases of ovulatory cycles in normal women. Plasma estradiol was lower (mean +/- SE, 52 +/- 5 pg/ml) than either cycle stage in normal women. Mean plasma LH was lower than EF values and FSH was higher than LL values. The amplitude of LH pulses in HA was similar to that in normal women. LH pulse frequency was the same as that present during the LL, but lower than that during the EF (HA, 4.7 pulses/12 h; EF, 7.7 pulses/12 h; P less than 0.05). In addition to the similar frequency, the patterns of LH secretion in HA resembled that of LL in that the amplitude of LH pulses was highly variable and pulses occurred at irregular intervals. Consistent changes in diurnal gonadotropin secretion were not found, and LH secretion was greater at night in 9 studies and during the day in 5 studies. Repeat studies in three patients (5-13 months later) revealed that LH pulse frequency was variable, being unchanged in 1, increased in 1, and decreased in the third patient. Thus, LH pulse frequency and, by inference, GnRH pulse frequency are similar in HA to those in the normal luteal phase despite a different steroid milieu. GnRH pulse frequency increases from the luteal to the follicular phases of normal cycles and may be important in the initiation of ovarian follicular maturation. These data suggest that the absence of cyclical gonadotropin secretion and anovulation in HA result from a decreased frequency and irregular amplitude of GnRH secretion and consequent absence of ovarian follicular maturation.

Adolescent↗
PubMed1987

Atrial natriuretic polypeptide inhibits cortisol secretion as well as aldosterone secretion in vitro from human adrenal tissue.

The effect of alpha-human atrial natriuretic polypeptide (ANP) on adrenal steroidogenesis was studied in human adrenal tissues obtained surgically from four patients with Cushing's syndrome due to an adrenal adenoma and five patients with an aldosterone-producing adenoma (APA). ANP significantly inhibited basal and ACTH (3.4 X 10(-8) M)-stimulated cortisol and aldosterone secretion in both the adenomas and adjacent adrenocortical tissues from patients with Cushing's syndrome. ANP inhibited ACTH-stimulated, but not basal, secretion of cortisol and aldosterone in the adjacent tissues from patients with APA. In addition, ANP significantly inhibited both basal and ACTH-, angiotensin II (10(-6) M)-, and potassium chloride (10 mM)-stimulated secretion of aldosterone from the adenomas of patients with APA. ANP-induced changes in cortisol and aldosterone secretion were accompanied by a decrease in cAMP and an increase in cGMP secretion. These results suggest that ANP may be a possible regulator of cortisol as well as aldosterone secretion in humans, and these effects might be due to concomitant alteration in cyclic nucleotide metabolism.

Adenoma↗
PubMed1988

Dopaminergic regulation of alpha-subunit secretion and messenger ribonucleic acid levels in alpha-secreting pituitary tumors.

Glycoprotein hormone and/or subunit secretion has been increasingly recognized in patients with pituitary nonsecretory adenomas and alpha-subunit secretion has been reported to occur in 5-10% of all pituitary tumors. We investigated the dopaminergic regulation of alpha-subunit secretion in four patients with alpha-subunit secreting pituitary adenomas documented by serum and immunocytochemical studies. In three of the four patients there was a significant decrease in serum alpha-subunit concentrations during 6 weeks of bromocriptine administration. Tumor size decreased in two patients. In pituitary tumor cells from one patient cultured in vitro, dopamine caused a highly significant decrease in media alpha-subunit concentrations. To investigate whether dopaminergic regulation of alpha-subunit secretion occurs at a pre- or posttranslational level, messenger RNA (mRNA) from cultured tumor cells from one patient was analyzed by Northern blot techniques. A decrease in alpha-subunit mRNA occurred in cells incubated with 10(-10), 10(-8), and 10(-6) M dopamine. We conclude that dopamine suppressed pituitary tumor alpha-subunit secretion and mRNA levels. Dopamine agonists may be of benefit in the therapy of patients with such tumors.

Adenoma↗
PubMed1980

The secretion of the eggshell of Schistocerca gregaria: ultrastructure of the follicle cells during the termination of vitellogenesis and eggshell secretion.

The secretion of the eggshell by the follicle cells in the desert locust, Schistocerca gregaria, was studied using the electron microscope. The 3 layers of the eggshell, the vitelline membrane, the endochorion, and the exochorion, are produced in sequence over a short period of about 30-36 h. The follicle cells contain little rough endoplasmic reticulum (RER) and small inconspicuous Golgi bodies during vitellogenesis. As eggshell secretion approaches there is an increase in the amount of RER and Golgi cisternae contain electron-dense product. At each stage of the 3-phase secretion cycle the follicle cells contain Golgi bodies and secretion vesicles with distinct morphology. The follicle cells increase in breadth and decrease in height between the beginning and end of eggshell secretion. The endochorion ridges arise at the junction between follicle cells and appear to be moulded by the microvilli formed at this position. In the ovary prior to ovulation, the eggshell consists of a thin (0.5 micrometer) electron-dense vitelline and an outer fibrillar exochorion layer, 20-30 micrometer thick. Further changes take place in the vitelline membrane and the endochorion after oviposition, and a layer of curly fibres, the extrachorion, is secreted in the oviduct.

Animals↗
PubMed1999

Tumor necrosis factor alpha inhibition of follicle-stimulating hormone-induced granulosa cell estradiol secretion in the human does not involve reduction of cAMP secretion but inhibition at post-cAMP site(s).

Tumor necrosis factor alpha (TNF) inhibits follicle-stimulating hormone- (FSH)induced estradiol secretion by granulosa cells in several species, including humans. One major inhibitory effect of TNF in rat granulosa cells is at the level of stimulatable adenylyl cyclase, resulting in reduced cAMP concentrations. The purpose of the present study was to investigate whether a reduction in cAMP secretion could account for the inhibitory effects of TNF on FSH-induced estradiol in human granulosa cells. Granulosa cells were taken from ovaries of premenopausal women undergoing oophorectomy for reasons unrelated to ovarian pathology. Women in this study were in various stages of the menstrual cycle or exhibited irregular cycles. Granulosa cells from follicles ranging from 5 to 10 mm diameter were subjected to culture for 48 and 96 h. Granulosa cells were cultured with human FSH (2 ng/mL) and testosterone (1 microM) in the presence and absence of human TNF (20 ng/mL). Media were collected at 48 h, fresh media and hormones added, and cultures continued for an additional 48 h. Accumulation of cAMP, progesterone, and estradiol in media were determined by radioimmunoassay (RIA). FSH induced significant increases in cAMP, progesterone, and estradiol by 96 h of culture. TNF inhibited the secretion of estradiol at 96 h without reducing the accumulation of cAMP and progesterone in media. Similar results were observed in the presence of 0.1 mM isobutylmethylxanthine (D3MX), a phosphodiesterase inhibitor that would prevent metabolism of cAMP to AMP. To determine whether TNF would inhibit the ability of cAMP to induce estradiol and progesterone secretion, granulosa cells were incubated with 0.1 mM cAMP in the presence and absence of TNF. TNF consistently inhibited the ability of cAMP to increase estradiol secretion. These results indicate that a pathway for TNF inhibition of FSH- or cAMP-induced estradiol secretion in human granulosa cells is at post-cAMP sites rather than inhibition of FSH-stimulatable adenylyl cyclase.

1-Methyl-3-isobutylxanthine↗
PubMed1990

Growth hormone secretion patterns in relation to LH and testosterone secretion throughout normal male puberty.

Pulsatile growth hormone secretion patterns were studied in relation to LH and testosterone release in 30 healthy prepubertal boys and 2 adult men. Plasma GH was measured every 10 min, plasma LH and testosterone every hour. Night-time GH secretion parameters were 2-3 times higher than daytime values. During daytime, mean GH level and the fraction of GH in pulses increased from Tanner stage G2 to G4 (p = 0.01); during night-time these parameters increased as well (p less than or equal to 0.1) and decreased from stage G5 to adulthood (p = 0.05). GH pulse number did not increase; the number of high-amplitude (greater than 8 micrograms/l pulses, however, increased from stage G2 to G4 (p = 0.05) during the day. Height velocity correlated with their number of high pulses during day and night (tau = 0.39, p less than 0.003). From stage G2 to G4 significant correlations were observed between nocturnal testosterone levels and GH secretion parameters (tau = 0.53-0.57), in contrast to nocturnal LH levels. It is concluded that during puberty 1. GH secretion increases as a result of an increased pulse amplitude; 2. there is no consistent correlation between GH and LH levels; 3. increasing nocturnal testosterone levels are correlated with the increasing GH secretion; therefore GnRH does not seem to influence GH secretion directly, but an indirect effect via testosterone is more conceivable, and 4. height velocity is correlated with the number of high GH pulses.

Adolescent↗
PubMed1991

Patterns of spontaneous pulsatile secretion of human chorionic gonadotropin and pregnancy specific beta 1 glycoprotein by superfused placental explants in first and last trimester. Lack of episodic human placental lactogen secretion.

We have recently reported that during superfusion of placental explants, human chorionic gonadotropin secretion is episodic. In the present work we have examined, using the superfusion model, the pattern of secretion of other glycoprotein hormones, pregnancy specific beta 1 glycoprotein and human placental lactogen, in the first trimester and term placenta. This was done by evaluating the pulsatile pattern by two different computerized programmes. By using different sampling intervals (6-0.5 min) of the effluent, two distinct patterns of hCG secretion were detected in the first trimester: a short one, occurring every 8-9 min and the other every 18-25 min. In contrast, at term the only episodic pattern detected was every 40-50 min, with a low amplitude, 20-30% above baseline, and a declining baseline. In two out of seven placentas, no pulsatility was detected. The secretion of pregnancy specific beta 1 glycoprotein was pulsatile, occurring every 14-15 min in the first trimester and every 6-7 min at term. Finally, the secretion of human placental lactogen at term was not pulsatile. The levels of this glycoprotein in the first trimester placenta were below detection limits. In conclusion, the patterns of the three glycoproteins during superfusion are different, suggesting different paracrine/autocrine control mechanisms. The dynamic superfusion model also enables identification of thus far not reported gestational age-dependent differences in the secretion pattern of hCG and pregnancy specific beta 1 glycoprotein.

Chorionic Gonadotropin↗
PubMed1997

Pyridostigmine treatment selectively amplifies the mass of GH secreted per burst without altering GH burst frequency, half-life, basal GH secretion or the orderliness of GH release.

Growth hormone (GH) release from the anterior pituitary gland is predominantly regulated by the two antagonistic hypothalamic peptides, growth hormone-releasing hormone (GHRH) and somatostatin. Appraising endogenous GHRH action is thus made difficult by the confounding effects of (variable) hypothalamic somatostatin inhibitory tone. Accordingly, to evaluate endogenous GHRH actions, we used a clinical model of presumptively acute endogenous somatostatin withdrawal with concomitant GHRH release. To this end, we administered in randomized order placebo or the indirect cholinergic agonist, pyridostigmine, for 48 h to 13 healthy men of varying ages (29-77 years) and body mass indices (21-47 kg/m2). We sampled blood at 10-min intervals for 48 h during both placebo and pyridostigmine (60 mg orally every 6 h) administration, and used an ultrasensitive GH chemiluminescence assay (sensitivity 0.0002-0.005 microgram/l) to capture GH pulse profiles. Multiparameter deconvolution analysis was applied to quantitate the number, amplitude, mass, and duration of significant underlying GH secretory bursts, and simultaneously estimate the GH half-life and concurrent basal GH secretion. Approximate entropy was utilized as a novel regularity statistic to quantify the relative orderliness of the hormone release process. All measures of GH secretion/half-life and orderliness were statistically invariant across the two consecutive 24-h placebo sessions. In contrast, pyridostigmine treatment significantly increased the mean serum GH concentration from 0.23 +/- 0.054 microgram/l during placebo to 0.45 +/- 0.072 microgram/l during the first day of treatment (P < 0.01). There was also a significant rise in the calculated 24-h pulsatile GH production rate from 8.9 +/- 1.7 micrograms/l/day on placebo to 27 +/- 5.6 micrograms/l/day during active drug treatment (P < 0.01). Pyridostigmine significantly and selectively amplified GH secretory burst mass to 1.5 +/- 0.35 micrograms/l compared with 0.74 +/- 0.19 microgram/l on placebo (P < 0.01). This was attributable to stimulation of GH secretory burst amplitude (maximal rate of GH secretion attained within the release episode) with no prolongation of estimated burst duration. Basal GH secretion and approximate entropy were not altered by pyridostigmine. However, age was strongly related to more disorderly GH release during both days of pyridostigmine treatment (r = +0.79, P = 0.0013). During the second 24-h of continued pyridostigmine treatment, most GH secretory parameters decreased by 15-50%, but in several instances remained significantly elevated above placebo. Body mass index, but not age, was a significantly negative correlate of the pyridostigmine-stimulated increase in GH secretion (r = -0.65, P = 0.017). In summary, assuming that somatostatin is withdrawn and (rebound) GHRH release is stimulated via pyridostigmine administration, we infer that relatively unopposed GHRH action principally controls GH secretory burst mass and amplitude, rather than apparent GH secretory pulse duration, the basal GH secretion rate, or the serial regularity/orderliness of the GH release process in the human. Moreover, we infer that increasing age is accompanied by greater disorderliness of somatostatin-withdrawn GHRH, and hence rebound GH, release. The strongly negative correlation between pyridostigmine-stimulated GH secretion and body mass index (but not age) further indicates that increased relative adiposity may result in decreased effective (somatostatin-withdrawn) endogenous GHRH stimulus strength.

Adult↗
PubMed1992

Suppression of pulsatile luteinizing hormone secretion by gonadotrophin-releasing hormone antagonist does not affect episodic progesterone secretion or corpus luteum function in ewes.

Progesterone secretion has been observed to be episodic in the late luteal phase of the oestrous cycle of ewes and is apparently independent of luteinizing hormone (LH). This study investigated the effects of suppressing the pulsatile release of LH in the early or late luteal phase on the episodic secretion of progesterone. Six Scottish Blackface ewes were treated i.m. with 1 mg kg-1 body weight of a potent gonadotrophin-releasing hormone (GnRH) antagonist on either day 4 or day 11 of the luteal phase. Six ewes received saline at each time and acted as controls. Serial blood samples were collected at 10 or 15 min intervals between 0 and 8 h, 24 and 32 h, and 48 and 56 h after GnRH antagonist treatment and daily from oestrus (day 0) of the treatment cycle for 22 days. Oestrous behaviour was determined using a vasectomized ram present throughout the experiment. Progesterone secretion was episodic in both the early and late luteal phase with a frequency of between 1.6 and 3.2 pulses in 8 h. The GnRH antagonist abolished the pulsatile secretion and suppressed the basal concentrations of LH for at least 3 days after treatment. This suppression of LH, in either the early or late luteal phase, did not affect the episodic release of progesterone. Daily concentrations of progesterone in plasma showed a minimal reduction on days 11 to 14 after GnRH antagonist treatment on day 4, although this was significant (P < 0.05) only on days 11 and 13. There was no effect of treatment on day 11 on daily progesterone concentration, and the timing of luteolysis and the duration of corpus luteum function was unaffected by GnRH antagonist treatment on either day 4 or day 11. These results indicate that the episodic secretion of progesterone during the luteal phase of the oestrous cycle in ewes is independent of LH pulses and normal progesterone secretion by the corpus luteum can be maintained with minimal basal concentrations of LH.

Analysis of Variance↗
PubMed1993

Maturational changes in gonadotrophin secretion: the LH response to realimentation and a nocturnal increment in LH secretion of feed-restricted prepubertal gilts.

Potential maturational changes in patterns of LH secretion during feed restriction and the LH response to realimentation were examined. Ten sets of four growth-matched littermate gilts were fed ad libitum, to reach either 55, 65, 75 or 85 kg target body weights (one littermate per weight). Gilts were then maintenance fed for 8 days (days 1-8), and to appetite on day 9, and kept in a 9 h light (07:00-16:00 h):15 h dark photoperiod. Blood samples were obtained every 10 min from 07:00 to 16:00 h, and from 16:00 to 24:00 h on day 8 to evaluate any nocturnal rise in LH, and from 07:00 to 16:00 h on day 9 to evaluate the LH response to realimentation. Radioimmunoassays for LH, FSH, melatonin and oestradiol were performed on selected plasma samples. In all three sampling periods, LH and FSH secretion decreased as gilt weight increased, in a quadratic manner. During feed restriction, daytime LH, but not FSH, secretion was lower than at nighttime, irrespective of weight. Daytime LH secretion increased in response to realimentation, irrespective of weight. Plasma oestradiol concentrations were increased by feed restriction and decreased by realimentation but showed little relationship to gilt weight. No consistent relationship was established between plasma melatonin concentrations and ambient illumination. In conclusion, LH secretion exhibits a diurnal rhythm during feed restriction in the prepubertal gilt and, in a similar way to FSH, decreases as puberty is approached. The plane of nutrition influences circulating oestrogen concentrations. The increase of LH secretion following realimentation is not influenced by maturation over the prepubertal period.

Animals↗
PubMed1993

Epidermal growth factor acts directly on the sheep ovary in vivo to inhibit oestradiol-17 beta and inhibin secretion and enhance progesterone secretion.

Epidermal growth factor (EGF) is a potential intra-ovarian modulator of gonadotroph action on differentiated follicular cells. Specific binding sites have been identified in the ovary and functional differentiation in cultured granulosa cells can be modulated by treatment with EGF. The aim of this study was to determine if EGF was capable of altering ovarian function in vivo during the follicular phase of the sheep oestrous cycle. Fourteen cross-bred ewes with ovarian autotransplants were treated with progestagen pessaries for 12 days. Three ewes were infused with murine EGF (mEGF) via the jugular vein (75 micrograms/kg bodyweight per 12 h) during the 12 h preceding progestagen pessary withdrawal, and received an injection of a prostaglandin analogue at 0 h to induce luteolysis. Over the same time-period, two doses of EGF were administered to other groups of ewes by infusion into the ovarian artery (low: 6 micrograms/12 h, n = 3 and high: 60 micrograms/12 h, n = 3). The remaining five ewes were not infused with EGF (controls). Jugular and ovarian venous blood samples were taken at 10-min intervals at two stages during the follicular phase (21-27 h and 38-42 h after pessary withdrawal) and every 2 h from 44 to 76 or 86 h. mEGF, LH, FSH, inhibin, androstenedione, oestradiol-17 beta and progesterone concentrations in plasma were determined using radioimmunoassays. The secretion rates of androstenedione, oestradiol, progesterone and inhibin by the ovary were calculated. EGF acted directly on the ovary in a dose-dependent manner. Oestradiol secretion was inhibited following treatment with EGF but androstenedione secretion was unaffected. EGF appears therefore to act within the granulosa cells to inhibit aromatization. Inhibin secretion was also suppressed by treatment with EGF, though it was not possible to determine if this was caused by a direct or indirect action of EGF on granulosa cells. The rate of progesterone secretion increased in ewes receiving systemic (i.e. via the jugular vein) and high-dose intra-arterial infusions of EGF, even though a preovulatory LH surge was not observed in these animals during the entire experimental period. Concomitant increases in both LH and FSH secretion were associated with these effects of EGF on ovarian function. In conclusion, EGF appears to act directly on the granulosa cells of the follicle to inhibit aromatization and also to inhibit inhibin production. The low levels of oestradiol and inhibin in the presence of high levels of gonadotrophin indicate that atresia may have been induced in medium to large antral follicles.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1997

Pulsatile secretion of alpha-MSH and the differential effects of dexamethasone and haloperidol on the secretion of alpha-MSH and ACTH in dogs.

This study was performed to determine whether, in the dog, there is at any time pulsatile release of alpha-MSH and whether secretion of ACTH from the pars intermedia (PI) contributes to the circulating concentrations of ACTH. The 24-h secretory profiles of alpha-MSH, ACTH, and cortisol were determined in eight dogs. Plasma samples were obtained at 10-min intervals via an indwelling jugular catheter during two 12-h periods. Pulsatile secretion of alpha-MSH was found in all dogs, with wide variations in peak height. Plasma alpha-MSH levels were usually low (mean 15 pmol/l), but brief, distinct periods of increased plasma alpha-MSH concentrations as high as 489 pmol/l were found. Analysis of pulse frequency revealed a mean of 4.75 significant alpha-MSH peaks/24 h. The highest alpha-MSH peaks were associated with definite changes in the plasma concentrations of ACTH. In separate studies, the influence of dexamethasone on the 6-h secretory profiles and on the haloperidol-stimulated secretion of alpha-MSH, ACTH, and cortisol was investigated. In these two studies, plasma ACTH was measured by a highly sensitive immunoradiometric assay. Dexamethasone pretreatment significantly suppressed the plasma concentrations of ACTH, cortisol, and alpha-MSH to 10.3%, 3.9%, and 74.6% respectively. Dexamethasone pretreatment also significantly reduced the haloperidol-stimulated secretion of ACTH and cortisol, but had no influence on the haloperidol-stimulated secretion of alpha-MSH. After the administration of haloperidol to the dexamethasone-pretreated dogs, there were small increases in the plasma concentrations of ACTH and cortisol, the latter being significant. These data demonstrate that alpha-MSH is secreted spontaneously in a pulsatile manner in the dog and suggest that the canine PI contributes to circulating ACTH concentrations.

Adrenocorticotropic Hormone↗
PubMed1991

Gastric bicarbonate secretion, acid secretion, and mucosal blood flow during influence of pentagastrin and omeprazole in the cat.

In this study secretion of bicarbonate and acid and mucosal blood flow were determined simultaneously in cats. The gastric lumen of anesthetized cats was continuously perfused with isotonic saline. Secretion of HCO-3 and H+ was calculated from continuous measurements of pH and PCO2 in the perfusate. Mucosal blood was measured by means of radiolabeled microspheres. Under resting acid secretory conditions, bicarbonate secretion into the gastric lumen averaged 1.0 mumol/min. Somewhat surprising, both omeprazole (4 mg/kg as bolus) and pentagastrin (16 micrograms/kg.h intravenously) significantly reduced the HCO-3 secretion. Omeprazole did not influence mucosal blood flow, whereas corpus mucosal blood flow increased during pentagastrin stimulation. Under resting acid secretory conditions and during omeprazole treatment there was a close linear relationship between acid and bicarbonate secretion. No such relationship was found during pentagastrin stimulation of the mucosa. No consistent relationship was obtained between blood flow and bicarbonate secretion in normal gastric mucosa.

Animals↗
PubMed2002

Secretion of Pem-CMG, a peptide in the CHH/MIH/GIH family of Penaeus monodon, in Pichia pastoris is directed by secretion signal of the alpha-mating factor from Saccharomyces cerevisiae.

The CHH/MIH/GIH peptide family of black tiger prawn (Paneaus monodon) is important in shrimp reproduction and growth enhancement. In this study, the cDNA that encodes the complete peptide that is related to the CHH/MIH/GIH family (so-called, Pem-CMG) in the eyestalk of P. monodon was successfully expressed in a methylotrophic yeast Pichia pastoris under the control of an alcohol oxidase promoter. In order to obtain the secreted Pem-CMG, a secretion signal of either the Saccharomyces cerevisiae alpha-factor or Pem-CMG was employed. The results demonstrated that alphaPem-CMG, either with (alpha2EACMG) or without (alphaCMG) the Glu-Ala repeats, was secreted into the medium, while Pem-CMG with its own secretion signal failed to be secreted. The total protein amount that was secreted from the transformant that contained either alpha2EACMG or alphaMG was approximately 60 mg/l and 150 mg/l, respectively. The N-terminus of the Pem-CMG peptide of both alpha2EACMG and alphaCMG was correctly processed. This produced the mature Pem-CMG peptide.

Animals↗
PubMed1991

1 alpha,25-dihydroxyvitamin D3 stimulates synthesis and secretion of nonphosphorylated osteopontin (secreted phosphoprotein 1) in mouse JB6 epidermal cells.

Murine JB6 epidermal cells can be irreversibly transformed into tumorigenic cells by the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate. One feature of this transformation is induction of the synthesis and secretion of the phosphoprotein osteopontin (also called secreted phosphoprotein 1 and previously referred to as transformation-related phosphoprotein, 2ar, bone sialoprotein 1, or Mr 44,000 bone phosphoprotein), an arginylglycylaspartic acid-containing cell adhesion glycoprotein the expression of which has been implicated in tumorigenesis and metastasis. Since 1 alpha,25-dihydroxyvitamin D3, calcitriol, also transforms JB6 cells and, in other cell types, regulates osteopontin synthesis, we hypothesized that calcitriol-mediated transformation of JB6 cells would also cause induction of osteopontin synthesis and secretion. Metabolic labeling with 32PO4 of near confluent JB6 cells (clone 41.5a) treated with calcitriol (0.1-100 ng/ml) for up to 48 h revealed only a minimal production of osteopontin, which is the major phosphoprotein secreted by 12-O-tetradecanoylphorbol-13-acetate-treated cells. Similar treatment followed by labeling with [35S]methionine showed a substantial dose-dependent increase in the synthesis and secretion of osteopontin. This induction was not associated with increased cell proliferation or with cell transformation, as assayed by anchorage-independent growth. Calcitriol-treated cells were morphologically indistinguishable from control cells, while 12-O-tetradecanoylphorbol-13-acetate-treated cells acquired a distinctive morphology. No induction of osteopontin was found with 25-hydroxyvitamin D3 or 24R,25-dihydroxyvitamin D3. These results show that calcitriol induces the synthesis and secretion of a nonphosphorylated form of osteopontin, in a cell type which normally makes little or none of this protein, and that the induction is not correlated with the tumorigenic transformation of these cells.

Animals↗