Regulation Of Anterior Pituitary Function Research Articles

Gonadotropin-releasing hormone and gonadal steroids regulate transcription factor mRNA expression in primary pituitary and immortalized gonadotrope cells.

Hormonal regulation of pituitary gonadotropin gene expression has been attributed to gonadotropin-releasing hormone (GnRH)-mediated stimulation of immediate early gene expression and gonadal steroid interactions with their respective nuclear receptors. A number of orphan nuclear receptors including steroidogenic factor 1, liver receptor homologue 1, dosage-sensitive sex reversal, adrenal hypoplasia critical region, on chromosome X, gene 1, and chicken ovalbumin upstream promoter-transcription factors I/II as well as the GATA family members, GATA2 and GATA4, have also been implicated in transcriptional regulation of the gonadotropin genes. We hypothesized that hormonally mediated changes in these latter transcription factors may provide an additional mechanism for mediating hormonal effects beyond the more classically appreciated pathways. In these studies, we demonstrate significant regulation of orphan nuclear receptor and GATA messenger RNA levels by GnRH, dihydrotestosterone, estradiol, and progesterone in both cultured primary pituitary cells and gonadotrope-derived cell line, LβT2. These results advance our understanding of the complex mechanisms by which GnRH and steroid hormones achieve precise regulation of anterior pituitary function.

Functional expression of CXCR4 in somatotrophs: CXCL12 activates GH gene, GH production and secretion, and cellular proliferation

The interaction of chemokine (C-X-C motif) ligand 12 (CXCL12) and its receptor CXCR4 may play an important role in the regulation of anterior pituitary function. In this study, we investigated the expression of CXCL12 and CXCR4 and their role in normal rat pituitary and GH-producing GH3 tumor cell line. RT-PCR analysis and immunohistochemistry revealed that CXCR4 was expressed in normal rat anterior pituitary and GH3 tumor cells. Double immunofluorescent staining showed the complete colocalization of CXCR4 with GH in rat pituitary, indicating that CXCR4 is specifically expressed in rat somatotrophs. Using rat primary pituitary cell cultures and GH releasing hormone receptor expressing stable GH3 cells (GH3-GHRHR), we evaluated the function of CXCL12 compared with GHRH. CXCL12 stimulated GH gene activation in both primary rat anterior pituitary cells and GH3-GHRHR cells. CXCL12 also stimulated GH secretion from primary rat pituitary cells in a dose-dependant manner. BrdU incorporation was increased in response to CXCL12 addition in GH3 cell culture, indicating CXCL12-induced cell proliferation. CXCL12-dependent phosphorylation of ERK1/2 was also confirmed by western blot analysis, supporting the evidence that MAPK is an intracellular mediator of CXCL12/CXCR4 interaction in GH3 cell proliferation. In conclusion, these results indicate that CXCL12/CXCR4 interaction plays an important role in GH production, secretion, and the proliferation of somatotrophs.

Cocaine- and Amphetamine-Regulated Transcript Co-Contained in Thyrotropin-Releasing Hormone (TRH) Neurons of the Hypothalamic Paraventricular Nucleus Modulates TRH-Induced Prolactin Secretion

TRH synthesized in hypophysiotropic neurons of the hypothalamic paraventricular nucleus (PVN) stimulates the release of TSH and prolactin from the anterior pituitary gland. Recent data from our laboratories have demonstrated that TRH and cocaine- and amphetamine-regulated transcript (CART) are co-contained only in hypophysiotropic neurons in the PVN. To determine whether CART and TRH interact in the regulation of anterior pituitary function, we have studied the effects of CART on TRH-induced release of TSH and prolactin in anterior pituitary cell cultures, and the effects of hypo- and hyperthyroidism on CART mRNA in the PVN. Dispersed anterior lobe cells from male rats were treated with CART (10(-6), 10(-8), 10(-10), and 10(-12) m) or TRH (10(-7) m) alone and TRH (10(-7) m) combined with various concentrations of CART for 4 h at 37 C. The medium was assayed for prolactin and TSH by RIA. TRH resulted in a marked increase of both prolactin and TSH release, whereas CART had no effect on prolactin or TSH secretion. When the two peptides were used in combination, CART dose-dependently inhibited TRH-induced prolactin release but had no significant effect on TRH-induced TSH release. By semiquantitative analysis of in situ hybridization autoradiographs, CART mRNA was significantly elevated in hypothyroid animals, whereas a reduction in CART mRNA was observed in hyperthyroid animals compared with euthyroid controls. These data raise the possibility that CART expressed in hypophysiotropic TRH neurons has an important role in the modulation of TRH-induced prolactin secretion. Increased secretion of CART may be responsible for the reduced TRH-induced prolactin response during hypothyroidism.

Transgenic studies on the regulation of the anterior pituitary gland function by the hypothalamus

The anterior pituitary gland is composed of five different cell types secreting hormones whose functions include the regulation of post-natal growth (growth hormone, GH), lactation (prolactin, PRL), reproduction (luteinising hormone, LH, and follicle stimulating hormone, FSH), metabolism (thyroid stimulating hormone, TSH), and stress (adrenocorticotrophic hormone, ACTH). The synthesis and secretion of the anterior pituitary hormones is under the control of neuropeptides released from the hypothalamus into a capillary portal plexus which flows through the external zone of the median eminence to the anterior lobe. This review describes the ways that gene transfer technologies have been applied to whole animals in order to study the regulation of anterior pituitary function by the hypothalamus. The extensive studies on these neuronal systems, within the context of the physiological integrity of the intact organism, not only exemplify the successful application of transgenic technologies to neuroendocrine systems, but also illustrate the problems that have been encountered, and the challenges that lie ahead.

The effects of heroin on prolactin levels in male rhesus monkeys: use of cumulative-dosing procedures.

There is considerable evidence that mu opioid receptors are involved in the regulation of anterior pituitary function. For example, in nonhuman primates and humans, mu agonists generally increase prolactin (PRL) levels. In contrast, mu antagonists decrease or have no effect on PRL levels. The goal of this study was to assess the potential utility of cumulative-dosing procedures to evaluate the endocrine effects of mu opioid receptor ligands. The effects of single and multiple, cumulative doses of the mu agonist heroin and the mu-selective antagonist quadazocine on PRL levels were investigated in four male rhesus monkeys. Cumulative dose-response curves were determined by infusing increasing drug doses at 60 min intervals over 290 min. Blood samples for PRL analysis were collected at 25 and 50 min after each cumulative infusion. Samples were collected at similar time points following single drug dose administration. Heroin (0.01-0.32 mg/kg, IV) administration dose-dependently increased PRL levels. Maximum levels of heroin-induced PRL levels were equivalent after single and cumulative doses. Quadazocine alone (0.032-1.0 mg/kg, IM) did not alter PRL levels significantly. However, quadazocine (0.1 mg/kg, IM) antagonized heroin-stimulated increases in PRL levels and produced a significant rightward shift in the heroin dose-effect curve. These data suggest that a cumulative-dosing procedure similar to that used in behavioral pharmacology may be useful to study the endocrine pharmacology of mu opioids in rhesus monkeys.

The nuclear, 75 kDa form of early growth response protein-1/nerve growth factor-induced A protein is primarily restricted to LH beta-subunit-expressing cells in rat anterior pituitary.

Early growth response protein-1 (Egr-1)/nerve growth factor-induced A (also known as Zif-268, Krox-24, TIS8, ZENK) is a zinc-finger transcription factor which, although expressed in a range of organ systems, has been shown to be essential only in the maintenance of fertility through actions within the endocrine system. In the present study we have investigated the anatomical basis for actions of Egr-1 in the adult anterior pituitary gland. Using female rats and mice as experimental models, we have used immunocytochemical and microscopic analysis to make observations of the cellular and sub-cellular localization of Egr-1 protein. Immuno-(Western) blotting was first used to characterize the anterior pituitary proteins detected by a commercially available Egr-1 antibody. Subsequently, the antibody was used both singly and in combination with an LH beta-subunit antibody, for immunocytochemical localization studies in pituitary sections. The Egr-1 antiserum detected a single, major (primarily nuclear) 75 kDa protein band in Western blots of anterior pituitary extracts. Nuclear localization was confirmed by immunocytochemistry, which also demonstrated that the 75 kDa protein is localized to a minority sub-population of anterior pituitary cells in both rat and mouse. Dual immunocytochemical localization showed that the Egr-1 protein is primarily restricted to the nuclei of LH beta-subunit-expressing cells. Sub-cellular localization of Egr-1 to the nucleus is consistent with a direct role in transcriptional regulation of anterior pituitary function in the adult rat. Furthermore, a selective role in the physiological control of gonadotrophin gene expression is indicated.

Interaction between substance P and TRH in the control of prolactin release.

Substance P (SP) may participate as a paracrine and/or autocrine factor in the regulation of anterior pituitary function. This project studied the effect of TRH on SP content and release from anterior pituitary and the role of SP in TRH-induced prolactin release. TRH (10(-7) M), but not vasoactive intestinal polypeptide (VIP), increased immunoreactive-SP (ir-SP) content and release from male rat anterior pituitary in vitro. An anti-prolactin serum also increased ir-SP release and content. In order to determine whether intrapituitary SP participates in TRH-induced prolactin release, anterior pituitaries were incubated with TRH (10(-7) M) and either WIN 62,577, a specific antagonist of the NK1 receptor, or a specific anti-SP serum. Both WIN 62,577 (10(-8) and 10(-7) M) and the anti-SP serum (1:250) blocked TRH-induced prolactin release. In order to study the interaction between TRH and SP on prolactin release, anterior pituitaries were incubated with either TRH (10(-7) M) or SP, or with both peptides. SP (10(-7) and 10(-6) M) by itself stimulated prolactin release. While 10(-7) M SP did not modify the TRH effect, 10(-6) M SP reduced TRH-stimulated prolactin release. SP (10(-5) M) alone failed to stimulate prolactin release and markedly decreased TRH-induced prolactin release. The present study shows that TRH stimulates ir-SP release and increases ir-SP content in the anterior pituitary. Our data also suggest that SP may act as a modulator of TRH effect on prolactin secretion by a paracrine mechanism.

Cytokine expression and molecular mechanisms of their auto/paracrine regulation of anterior pituitary function and growth.

The pituitary gland expresses cytokines and their receptors. IL-2 receptor transcripts and protein products are co-localized in ACTH-, PRL-, and GH-producing cells (double immunofluorescence). IL-2 and IL-6 (1-1000 IU/ml) are involved in the autocrine/paracrine regulation of normal and tumor (GH3 mammosomatotroph cell line and adenoma cell cultures) anterior pituitary hormone-producing cell growth (cell number, DNA synthesis, c-fos mRNA expression and autoradiography combined with hormone staining). IL-1 regulates the growth of normal pituitary cells but does not act on GH3 cells. IL-1ra, which blocks this action, is expressed in tumoral pituitary (mainly GH- and ACTH-) cells. In ACTH- cells, IL-1 enhances glucocorticoid feedback, stimulating glucocorticoid response element transcriptional activity. Cytokines, through specific functional receptors, act as inter/auto-cellular factors that regulate not only the function but also the growth of anterior pituitary cells.

Bombesin Regulation of Adrenocorticotropin Release From Ovine Anterior Pituitary Cells

AU, C. L., B. J. CANNY, P. G. FARNWORTH AND A. S. GIRAUD.Bombesin regulation of adrenocorticotropin release from ovine anterior pituitary cells.PEPTIDES 18(7) 995–1000, 1997.—Mammalian members of the bombesin-like peptide family (gastrin releasing peptides; GRP) have been localized in the ovine median eminence and in hypophysial-portal blood, suggesting a role in the regulation of anterior pituitary function. In this study we have shown that although bombesin cannot stimulate ACTH secretion alone, it potentiates release by ovine CRF, an effect blocked by the GRP receptor antagonist d-Tyr6bombesin [6–13]propylamide. Bombesin did not potentiate AVP-stimulated ACTH release; instead release was attenuated when bombesin was given at a 10-fold or greater molar excess over AVP, with no interaction seen at lower concentrations. We conclude that ovine corticotrophs express bombesin receptors, and that GRP may act in concert with other hypothalamic releasing factors to regulate ACTH secretion.

Pregnancy Alterations Following Xenobiotic-Induced Delays in Ovulation in the Female Rat

Pregnancy Alterations Following Xenobiotic-Induced Delays in Ovulation in the Female Rat. Cooper. R. L., Barrett, M. A., Goldman, J. M., Rehnberg, G. L., McElroy, W. K., and Stoker, T. E. (1994). Fundam. Appl. Toxicol. 22, 474-480.Chlordimeform [N′-(4-chloro-o-tolyl)-N,N-dimethylformamidine] has been shown to cause a 1-day delay in the surge of luteinizing hormone (LH) in ovariectomized, steroid-primed female rats, presumably through its ability to block CNS α-noradrenergic receptors and consequently CNS regulation of anterior pituitary function. In the present study, we determined whether a chlordimeform-induced delay in the ovulatory surge of LH would alter pregnancy outcome in intact females. Chlordimeform (50 mg/kg) or sodium pentobarbital (35 mg/kg), as a positive control, was administered in order to delay ovulation 24 (1-day delay) or 48 hr (2-day delay). Females were then housed with proven fertile males on the evening of proestrus (0-day delay group), the following evening (1-day delay group), or the evening after that (2-day delay group). The number of receptive females in each group, the mean lordosis quotient, and the number of sperm-positive females in each group were recorded. All females were killed on Gestation Day 20. The number of pregnant females in the 1- or 2-day delay groups was reduced with both chlordimeform and pentobarbital. Also, delaying ovulation for 1 or 2 days with either compound resulted in a significant reduction in the number of live pups present on Gestation Day 20 and a decrease in the number of implantation sites. Litter size was not affected if the females were mated on the same day that treatment was administered (0-day delay). Pentobarbital did not alter the proportion of females showing sexual behavior or the mean lordosis quotient in the 0- and 1-day delay groups, although fewer 1-day females were sperm positive. The number of sexually active and sperm-positive females was reduced in the 2-day pentobarbital-delayed group. However, the lordosis quotient of those that were sexually active was not different than that of control. Similarly, in CDF-treated groups, the proportion of females showing sexual activity was reduced in the 0- and 2-day delayed groups. In contrast, sexual behavior was lower in the 0-day delayed females when tested 2 hr after lights out. These females did eventually mate, however, as confirmed by the high incidence of sperm positive smears the following morning. The number of sperm positive females was lower in both the 1- and 2-day chlordimeform-induced delay groups. Thus, brief exposures to compounds such as formamidine pesticide chlordimeform will result in not only a delay in breeding but, more importantly, a significant reduction in litter size.

Gonadotropin-Releasing Hormone and Its Receptors in Rat Brain

Since the chemical identification of gonadotropin-releasing hormone (GnRH) in 1971, significant progress has been made in understanding the mechanisms by which GnRH action is mediated in the anterior pituitary. In contrast, relatively little information is available which identifies the intracerebral sites and mechanisms of action of GnRH in the brain. Early immunohistochemical studies of GnRH distribution in the central nervous system, together with behavioral and electrophysiological experiments, suggested that GnRH functioned as a neurotransmitter and was, possibly, involved in the expression of reproductive behaviors. The subsequent identification and characterization of GnRH receptors in the brain further strengthened the view that GnRH caused specific effects in select regions of the brain known to be involved in the neuroendocrine regulation of the anterior pituitary and in the generation of reproductive behaviors. After the mouse pituitary GnRH receptor was cloned it became possible to identify brain neurons which contained the GnRH receptor mRNA. Comparison of the locations of the GnRH peptide, the GnRH receptor protein, and the neurons which contain the GnRH receptor mRNA suggests that the GnRH neuronal system itself can potentially provide a direct link between the neuroendocrine regulation of anterior pituitary function and the intracerebral regulation of reproductive behaviors; furthermore, it is possible that the GnRH neuronal system takes an active part in intracerebral feedback loop systems between the mediobasal hypothalamus and the septum-diagonal band which regulate GnRH release from the median eminence.

Endothelin-3 immunoreactivity in gonadotrophs of the human anterior pituitary.

Endothelin (ET), originally discovered in vascular endothelial cells, has also been demonstrated in nonvascular tissues. The present study was undertaken to elucidate the presence of ET in the human pituitary. The avidin-biotin complex method with antiserum to ET-1 (and ET-2) or ET-3 was used to identify ET in human pituitaries obtained by autopsy. ET-3 immunoreactivity was found in the cytoplasm of large ovoid cells of the anterior pituitary. Using the double staining method, the cells containing ET-3 immunoreactivity were differentiated from cells containing ACTH, TSH beta, GH, PRL, and protein S-100. By staining with anti-LH beta antiserum in adjacent sections and using the double staining method, the cells were identified as gonadotrophs. No staining was observed in the posterior pituitary. In addition, no ET-1 (and ET-2) immunoreactivity was detected. The specific localization of ET-3 immunoreactivity in the gonadotrophs of the human pituitary suggests a possible role of ET-3 in the regulation of anterior pituitary function.

Effect of Immunoneutralization of Neuropeptide Y on Gonadotropin and Prolactin Secretion in Normal Mice and in Transgenic Mice Bearing Bovine Growth Hormone Gene*

Immunoneutralization of endogenous neuropeptide Y (NPY) with specific antibodies was used to evaluate the possible physiological role of this neuropeptide in the regulation of gonadotropin and PRL secretion in the mouse. Because regulation of anterior pituitary function can be profoundly altered by chronic GH excess, we felt it was also of interest to have examined the effects of immunoneutralization of NPY in transgenic mice expressing bovine (b) GH gene with mouse metallothionein-I promotor. Intact or castrated transgenic and normal (nontransgenic) littermate adult male mice were injected with control rabbit serum or anti-NPY rabbit serum (anti-NPY). Blood samples were obtained 24 h later for hormone measurements. In intact transgenic mice expressing bGH gene, plasma LH levels were reduced and plasma PRL levels were increased, as compared to their normal littermates. Plasma levels of FSH were similar in normal and transgenic animals. Injection of anti-NPY increased plasma LH levels significantly in both intact normal and intact transgenic mice. However, plasma levels of FSH and PRL were increased significantly after anti-NPY treatment only in intact normal mice. In both normal and transgenic males, castration lead to the expected increase in plasma FSH and LH levels, whereas plasma levels of PRL remained unaltered. Administration of anti-NPY to castrated animals was followed by a significant increase in circulating LH levels in both transgenic and normal mice, whereas plasma levels of PRL were not changed. The results suggest that NPY plays a physiological role in the control of gonadotropin and PRL release in the adult male mouse, and that expression of the bGH gene in transgenic mice is associated with altered role of endogenous NPY in the control of pituitary function.

Neuroendocrine Aberrations in Women With Functional Hypothalamic Amenorrhea*

To further elucidate the neuroendocrine regulation of anterior pituitary function in women with functional hypothalamic amenorrhea (FHA), we measured serum LH, FSH, cortisol, GH, PRL, TSH concentrations simultaneously at frequent intervals for 24 h in 10 women with FHA and in 10 normal women in the early follicular phase (NC). Using the same data, we separately analyzed the cortisol-PRL responses to meals in these women. In addition, the pituitary responses to the simultaneous administration of GnRH, CRH, GHRH, and TRH were assessed in 6 FHA and 6 normal women. The 24-h secretory pattern of each hormone except TSH was altered in the women with FHA. Compared to normal women, the women with FHA had a 53% reduction in LH pulse frequency (P less than 0.0001) and an increase in the mean LH interpulse interval (P less than 0.01); LH pulse amplitude was similar. The 24-h integrated LH and FSH concentrations were reduced 30% (P = 0.01) and 19% (P less than 0.05), respectively. The mean cortisol pulse frequency, amplitude, interpulse interval, and duration were similar in the two groups, but integrated 24-h cortisol secretion was 17% higher in the women with FHA (P less than 0.05). This increase was greatest from 0800-1600 h, but also was present from 2400-0800 h. Cortisol levels were similar in the two groups from 1600-2400 h, resulting in an amplified circadian excursion. In contrast, the 24-h serum PRL levels were markedly lower at all times (P less than 0.0001), the sleep-associated nocturnal elevation of PRL was proportionately greater (P less than 0.05), and serum GH levels were increased at night in the women with FHA (P less than 0.05). Although 24-h serum TSH levels were similar at all times, T3 (P less than 0.05) and T4 (P less than 0.01) levels were lower in the FHA women. The responses of serum cortisol to lunch (P less than 0.01) and dinner (P less than 0.05) and those of serum PRL to lunch (P less than 0.05) and dinner (P = 0.08) were blunted in the women with FHA. Pituitary hormone increments in response to the simultaneous iv administration of GnRH, CRH, GHRH, and TRH were similar in the two groups, except for a blunted PRL response to TRH in the women with FHA (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Regulatory role of galanin in control of hypothalamic-anterior pituitary function.

The role of the neuropeptide galanin in the regulation of anterior pituitary function was studied in vivo in conscious male rats and in vitro with cultured anterior pituitary cells. Galanin (50-200 ng; 15-60 pmol) injected into the third cerebral ventricle of rats produced highly significant, dose-related increases of plasma growth hormone (GH) concentrations, whereas galanin increased prolactin (PRL) and decreased thyroid-stimulating hormone (TSH) levels only at the highest dose (60 pmol) tested. Intravenous galanin failed to alter PRL and TSH levels in these rats. In contrast with the results with intraventricular injection of the peptide, intravenous injection of 30 or 300 pmol of galanin produced small, brief, dose-related increases in plasma GH. The response to the 300-pmol dose was less than that induced by a factor-of-20-lower intraventricular dose, which establishes a central action of galanin. Galanin in concentrations ranging from 1 nM to 1 microM failed to alter significantly GH, PRL, or TSH release from dispersed anterior pituitary cells. It also failed to alter GH secretion in response to 100 nM GH-releasing hormone; however, at this dose galanin did potentiate the effect of 100 nM TSH-releasing hormone on TSH and PRL release. Thus, the effects of third-ventricular injection of the peptide are mediated by the hypothalamus. To determine the physiological significance of galanin in control of pituitary hormone release, highly specific antiserum against galanin was injected intraventricularly. Third-ventricular injection of 3 microliter of galanin antiserum resulted in a dramatic decrease in plasma GH values as compared with those of normal rabbit serum-injected controls within 15 min, which persisted until the end of the experiment (5 hr postinjection). Galanin antiserum did not decrease plasma PRL or TSH levels at any time period after its third-ventricular injection; however, a transient increase of plasma TSH levels occurred after 30 and 60 min in comparison with TSH levels in normal rabbit serum-injected controls. Since there was no effect of the antiserum on plasma PRL and only a transient elevation in TSH, galanin may not be physiologically significant enough during resting conditions to alter PRL and TSH release in the male rat. The results of the experiments with galanin antiserum indicate that endogenous galanin has a tonic action within the hypothalamus to stimulate GH release. The rapidity of onset of the effects of galanin and the antiserum directed against it suggest that it acts to stimulate release of GH-releasing hormone from periventricular structures, which then stimulates the release of GH.

The role of somatostatin in the regulation of anterior pituitary hormone secretion and the use of its analogs in the treatment of human pituitary tumors.

I. Introduction THE PRESENCE of GH-inhibitory substances in hypothalamic extracts was originally detected accidentally by Krulich et al. (1) during investigations into the distribution of GH-releasing factors throughout the rat hypothalamus. Several years later Brazeau et al. (2) isolated and characterized this somatotropin releaseinhibiting factor, called somatostatin (SRIF), which turned out to be a cyclic peptide consisting of 14 amino acids. SRIF was the first hormone to broaden the classic concepts of endocrinology because it has physiological effects both at the periphery and the central nervous system (3). Several reviews and proceedings from international symposia are available, which summarize the developments in the field of SRIF (4–12). In recent years SRIF analogs have been developed which can be used clinically. In the present review the physiological role of SRIF in the regulation of anterior pituitary function has been summarized as far as it contributes to the understanding of the use and ...

Neuroendocrine regulation of anterior pituitary function in patients during and after molar pregnancy.

Only partial studies evaluating the endocrine profile in molar pregnancy have been performed. In order to characterize the neuro-endocrine pattern during and after molar pregnancy, we studied the basal hormonal levels of hCG, human placental lactogen (hPL), FSH, GH, TSH, free thyroxine index (FTI), oestradiol-17 beta (E2), and progesterone (PG), as well as the anterior pituitary response to TRH, GnRH, and hypoglycaemia induced by insulin in 7 patients during molar pregnancy and one week after molar abortion. hCG showed significantly higher serum levels during rather than after molar pregnancy and hPL was detectable in only 4 patients during, but in none after molar pregnancy. FSH values were in the follicular phase range before and after molar abortion (12.7 +/- 0.8 and 12.7 +/- 3.5 IU/l). PRL had elevated basal levels before and after molar abortion; 103.0 +/- 16.5 and 43 +/- 10.6 micrograms/l, respectively (P less than 0.05). GH levels were distinctly elevated in 3 patients during molar pregnancy; after molar abortion, the basal GH values were normal in all patients less than 10 micrograms/l. Basal cortisol and TSH levels were in the normal range before and after molar abortion. The FTI was above the normal range in 3 patients during molar pregnancy, whereas after molar abortion the values were normalized. E2 levels were elevated before and after molar abortion, 1881 +/- 477 and 96.5 +/- 39.2 ng/l, respectively (P less than 0.01). PG levels before and after molar abortion were 30.9 +/- 5.4 and 10 +/- 6.7 micrograms/l, respectively (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Chapter 11 Neuropeptides and neurotransmitters involved in regulation of corticotropin-releasing factor-containing neurons in the rat

Publisher Summary The most potent hypothalamic hormone that regulates the release of adrenocorticotropic hormone (ACTH) from the pituitary gland is the corticotropin-releasing hormone (CRF). Vasopressin releases ACTH from the pituitary gland in vitro as well as in vivo . The possible role of cholecystokinin (CCK) in releasing pro-opiomelanocortin (POMC)-derived peptides from the anterior pituitary is investigated. CCK present in CRF neurons is assistant hormone in the control of ACTH release. The presence of vasoactive intestinal polypeptide (VIP) in portal blood indicates that VIP might be involved in the regulation of anterior pituitary function. Adrenal cortical steroids exert a negative feedback inhibition on the secretion of ACTH from the pituitary. CRF may be the most potent but not the only hypothalamic factor that releases ACTH from the anterior pituitary. The physiological, morphological, and biochemical studies are necessary to reveal all the structures and neurotransmitters involved in neuroendocrine regulation.

Substance P and Neurotensin: Their Roles in the Regulation of Anterior Pituitary Function

Mitochondrial fatty acid β-oxidation (FAO) is the major pathway for the degradation of fatty acids and is essential for maintaining energy homeostasis in the human body. Fatty acids are a crucial energy source in the postabsorptive and fasted states when ...Read More

Substance P and Neurotensin: Their Roles in the Regulation of Anterior Pituitary Function

Substance P and Neurotensin: Their Roles in the Regulation of Anterior Pituitary Function