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Biomedical subjects

S Reichlin

Publications and source records attributed to S Reichlin.

At least 73 records · Page 4Linked to original sources
PubMed1989

Neuroendocrinology of the pituitary gland.

The hypophysial-portal chemotransmitter hypothesis of control of the anterior pituitary was first set forth in the 1940s on the basis of physiological studies of the effects of lesions of the hypothalamus, and of section of the pituitary stalk on pituitary function. Morphological demonstration of specific neuropeptide pathways in the hypothalamus, which project to the median eminence, and the chemical identification of releasing hormones in the hypothalamus have fully established this theory. Specific neuropeptides have been isolated which stimulate the secretion of ACTH (CRF, corticotrophin releasing hormone), TSH (TRH, thyrotropin releasing hormone), GH (GHRH, growth hormone releasing hormone), and the gonadotropins (LHRH, luteinizing hormone releasing hormone; GnRH, gonadotropin releasing hormone). Prolactin secretion is regulated by both an inhibitory hormone (dopamine), and by one or more releasing factors. A factor inhibitory to GH and TSH secretion has also been identified. All factors except for the prolactin inhibitory hormone (which is a biogenic amine) are peptides, all synthesized as part of large prohormones. These substances have all been introduced into medical and veterinary practice where they are useful for regulation of pituitary abnormalities, and study of normal physiology.

Animals↗
PubMed1989

Interleukin-1 beta stimulates somatostatin biosynthesis in primary cultures of fetal rat brain.

Interleukin-1 (IL-1), a secretory product of activated macrophages and many other cell types, is an important mediator of the acute phase reaction to infection and to endotoxin administration. Previous reports that GH and TSH secretion are decreased following injection of endotoxin or IL-1 led us to test the hypothesis that IL-1 acts by releasing increased amounts of somatostatin (SS), a hypothalamic factor inhibitory of both GH and TSH release. Primary cultures of dispersed fetal rat diencephalic cells were found to contain increasing amounts of immunoreactive SS in both cells and media after addition of recombinant human IL-1 beta. This increase was detectable at 24 hours and continued for up to 6 days, the longest time interval tested. Increased content of SS peptide was accompanied by marked increases in SS mRNA. These changes were dose-related, the lowest effective dose being 10(-10) M. In contrast to the long term response, exposure of the cells to IL-1 beta for one hour had only minimal stimulating effects on somatostatin release. These data indicate that IL-1 beta is neurotrophic for the somatostatinergic neuron, an action that may be responsible at least in part, for the neuroendocrine response to infection.

Animals↗
PubMed1989

The peak phase of the proestrous prolactin surge is blocked by either posterior pituitary lobectomy or antisera to vasoactive intestinal peptide.

UNLABELLED: The proestrous surge of PRL could result from a decrease in dopamine, an increase in PRL-releasing factor (PRF) or both. The objectives were to determine whether PRF from the posterior pituitary regulates the proestrous PRL surge, and to examine if there are interactions between PRF and vasoactive intestinal peptide (VIP). Posterior pituitary lobectomy (LOBEX) and passive immunization against VIP were employed. Adult cycling rats were subjected at 0900 h on proestrus to LOBEX or sham surgery (SHAM) under short term anesthesia, and were injected iv at 1330 h with 0.75 ml anti-VIP serum or normal rabbit serum. Jugular blood was collected hourly from 1400-2300 h and analyzed for PRL and LH by RIA. Oviductal ova were examined on estrus. The rise in plasma PRL in normal rabbit serum-treated SHAM rats was biphasic, with an early peak between 1500-1700 h and a lower plateau between 1900-2100 h. This rise was similar in profile and magnitude to that seen in intact rats. In contrast, LOBEX significantly attenuated the early peak, but did not alter the plateau. Passive immunization against VIP of either SHAM or LOBEX rats mimicked the effect of LOBEX alone on PRL release. Neither surgery nor anti-VIP serum affected the profile of the LH surge which was sharp and symmetrical, and all rats ovulated with 15-16 ova per rat. To determine whether VIP is the posterior pituitary PRF, selected tissues removed on proestrus or diestrus-1 were analyzed for VIP by RIA. VIP was undetectable (less than 20 pg/organ) in the posterior pituitary on either day examined. The contents of VIP in the anterior pituitary, medial basal hypothalamus, and paraventricular nuclei were unchanged between diestrus-1 and proestrus. CONCLUSIONS: The proestrous surge of PRL consists of two components: an early peak and a late plateau. The peak phase appears to be dependent on PRF input from the posterior pituitary. This input might be regulated by VIP, and interactions between the two could occur at the level of the hypothalamus, anterior pituitary, or both. The plateau phase of the PRL surge is independent of the posterior pituitary and VIP, and might involve hypothalamic dopamine.

Animals↗
PubMed1989

Vasoactive intestinal peptide in the anterior pituitary is increased in hypothyroidism.

Vasoactive intestinal peptide (VIP) and PRL have been reported to be colocalized in rat lactotropes. To determine whether induced hypothyroidism, known to reduce pituitary PRL concentration, also reduces pituitary concentration of VIP, rats were treated with antithyroid drugs for 3 weeks. Pituitary PRL concentration in male rats (micrograms/mg protein) was markedly reduced by this treatment (9.4 +/- 1.0 vs. 2.3 +/- 0.4 when extracted at pH 1.1, 17.9 +/- 3.0 vs. 3.4 + 0.4 when extracted at pH 7.4, 21.8 +/- 3.3 vs. 6.7 + 1.3 when extracted at pH 10.0). Contrary to expectation, pituitary VIP concentration was markedly increased in hypothyroidism; in males from 169.5 +/- 20.3 to 834.0 +/- 82.2 pg/mg protein, and in females (whose pituitary PRL had been similarly reduced) from 103.1/I +/- 34.1 to 771.6 +/- 100.9 pg/mg protein. Serum PRL was significantly reduced in hypothyroid males (7.4 +/- 1.6 vs. 28.9 +/- 12.2 ng/ml) whereas in females, serum PRL was not significantly altered (41.4 +/- 11.6 vs. 38.8 +/- 14.3 ng/ml). The effect of hypothyroidism was reversed by administration of T4 in physiological doses. The authenticity of pituitary immunoreactive VIP was further established by demonstrating chromatographic patterns by Sephadex G-50 gel exclusion and reverse phase HPLC separations identical to synthetic VIP. Immunohistochemically reactive VIP cells could not be demonstrated in normal pituitaries, but the marked increase in VIP in hypothyroid animals made it possible to visualize a population of VIP immunoreactive stellate cells which appear to be distinct from hypothyroid lactotropes and thyrotropes.

Animals↗
PubMed1989

Synthesis and secretion of vasoactive intestinal peptide by rat fetal cerebral cortical and hypothalamic cells in culture.

To establish the neurosecretory activity of brain vasoactive intestinal peptide (VIP)ergic neurons and to characterize the molecular forms of secretion of these cells, fetal cerebrocortical and hypothalamic cells were grown in primary cultures for periods up to 4 weeks, their regulation by depolarization and calcium and sodium channel active agents was studied, and the chromatographic patterns of cell and medium VIP were determined. Mechanically dispersed cultured fetal telencephalic and diencephalic cells showed a progressive increase in immunoreactive VIP in both cells and media, reaching maximum values between 110-290 pg/mg protein.culture plate on days 15-20. Immunoreactive VIP in both cells and media corresponded almost exclusively to VIP-28 on exclusion chromatography and HPLC, and was identical to the form extracted from whole fetal brain. This indicates that both the stored and secreted forms of VIP are the mature 28-amino acid-containing peptide. To determine the influence of membrane depolarization on VIP release, the potassium concentration in the medium was increased to 30 and 56 mM, inducing a marked increase in medium VIP concentrations. The effects of K+ were dependent on Ca2+ transport, since release was blocked by the addition of verapamil, a Ca2+ channel blocker (20 microM). VIP release was stimulated by Na+ channel activation using the drug veratridine (100 microM); this effect was blocked by tetrodoxin. The influence of GH-releasing factor (GRF) on VIP release was studied by adding GRF (10(-9)-10(-7) M), alone or in the presence of anti-rGRF immunoglobulins (antirat GRF immunoglobulin G) to the incubation medium. Rat GRF stimulated VIP release and the simultaneous addition of antirat GRF immunoglobulin G blocked this effect. These findings confirm that VIP regulation by brain cells corresponds to the well defined patterns of membrane activation observed in other neuronal systems. They, furthermore, demonstrate that VIP release is under GRF influence.

Animals↗
PubMed1989

Thyroid hormone regulates vasoactive intestinal peptide (VIP) mRNA levels in the rat anterior pituitary gland.

Vasoactive intestinal peptide (VIP) is a secretagogue for pituitary prolactin, but the importance of this peptide in the normal control of prolactin secretion is unclear. Recent studies suggest VIP synthesis within the rat anterior pituitary. We have shown (Endocrinology 124:1077) that the content of rat pituitary VIP increases in hypothyroidism. To confirm in situ pituitary synthesis of VIP and determine whether thyroid hormone effects on pituitary VIP relate to changes in VIP mRNA, Northern and in situ hybridization analyses of VIP mRNA in rat pituitaries were performed. Northern hybridization demonstrated an RNA species from rat pituitary consistent with rat VIP mRNA. Hypothyroidism increased the content of pituitary VIP mRNA, and replacement with 1-thyroxine prevented this increase. In situ hybridization showed multiple, widely-distributed hybridizing cells in pituitaries from hypothyroid animals. A distinct population of VIP-producing pituitary cells exists which may serve to modulate prolactin secretion in a paracrine or autocrine fashion.

Animals↗
PubMed1989

The clinical and screening age-at-onset distribution for the MEN-2 syndrome.

The decision to screen for multiple endocrine neoplasia type 2 (MEN-2) is generally based on family history, the rationale for this approach being the presumed 100% penetrance of the disease. To determine the validity of this presumption we have estimated--by applying modifications of the life-table method--the clinical and screening age-at-diagnosis distributions for MEN-2, using families from the Cancer Research Campaign Medullary Thyroid Cancer Register and one large American family. The clinical penetrance of MEN-2 is shown to be incomplete, an estimated 41% of gene carriers not presenting with symptoms by age 70 on the basis of clinical history. Screening by the standard tests for detecting the earliest manifestations of the syndrome increases the penetrance to an estimated 93% by age 31. There is no evidence of a difference in the age-at-diagnosis distributions between maternal and paternal transmission, or among different families, but there is some suggestion of an earlier onset of medullary thyroid cancer in female gene carriers, and of a tendency of pheochromocytoma to cluster in families. These results can be used to calculate risks to relatives of affected individuals, which in turn can be used to guide decisions on which individuals to screen.

Adrenal Gland Neoplasms↗
PubMed1988

Adenylate cyclase activation is not sufficient to stimulate somatostatin release from dispersed cerebral cortical and diencephalic cells in glia-free cultures.

Under conditions in which vasoactive intestinal peptide (VIP) induces somatostatin release from cortical and diencephalic neuronal cultures, VIP causes large increases in intracellular cyclic AMP. Both the release of somatostatin and the increase in cyclic AMP elicited by VIP require exogenous calcium, can be blocked by cobalt ion, and can be qualitatively mimicked by depolarizating concentrations of exogenous potassium ion. Direct activation of adenylate cyclase by forskolin causes large increases in cyclic AMP content but does not induce somatostatin release. In the absence of VIP, the calcium ionophore, ionomycin, and the phorbol ester, phorbol 12-myristate-13-acetate, also stimulate somatostatin release. These results indicate that VIP-stimulation of cyclic AMP formation and VIP-stimulation of somatostatin release are calcium-dependent and that the two phenomena are dissociatable. Cyclic AMP formation is not a necessary condition for VIP-induced somatostatin release. Nucleotide formation may be a sufficient condition for release or, possibly in association with calcium influx, it may be an event unrelated to the release process.

1-Methyl-3-isobutylxanthine↗
PubMed1988

The clinical outcome of prospective screening for multiple endocrine neoplasia type 2a. An 18-year experience.

An important question facing physicians who care for families with multiple endocrine neoplasia type 2a is whether prospective screening to detect early abnormalities of the thyroid, parathyroid, or adrenal glands favorably influences the ultimate course of the disease. An 18-year study of a large family has allowed us to examine the effect of early treatment on the clinical course of the disease. Of 22 patients who underwent thyroidectomy for early C-cell abnormalities, 19 remained free of detectable medullary thyroid carcinoma according to all criteria, at a mean of 11 years after thyroidectomy. None of the 22 patients had evidence of parathyroid disease either at the time of surgery or after a mean follow-up of 10 years. Prospective screening for adrenal medullary abnormalities by means of measurement of 24-hour urinary epinephrine excretion and the ratio of urinary epinephrine to norepinephrine was predictive of pheochromocytoma in 10 of 11 patients (with a false negative result in one patient) but was not useful in diagnosing adrenal medullary hyperplasia. We conclude that regular, prospective screening and early treatment of the manifestations of multiple endocrine neoplasia can prevent metastasis of medullary thyroid carcinoma and the morbidity and mortality caused by pheochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1988

Neuroendocrine significance of vasoactive intestinal polypeptide.

The new data reported here, and available in the literature, are interpreted to indicate that acute release of PRL in stress is probably mediated by secretion of VIP and PHI arising from a subpopulation of paraventricular cells in the tuberoinfundibular system, and that this secretion is under serotonergic control, presumably by way of the raphe nuclear projection to the hypothalamus. The acute PRL response to suckling response is only partially under VIP/PHI control, and may be regulated by an as yet unidentified neural lobe hormone. In addition to the hypothalamic component of PRL regulation, there is a well-defined population of VIP cells within the pituitary, representing the only known example of VIP expression outside of nerve cells. This population of VIP cells is exquisitely responsive to thyroid status, and in common with the thyrotrope cell, is activated by hypothyroidism. Since VIP secretion is enhanced in the hypothyroid pituitary, and VIP release is stimulated by TRH, it is reasonable to postulate that paracrine VIP secretion may play a role in the reasonable to postulate that paracrine VIP secretion may play a role in the hyperprolactinemia prolactinemia that occurs in the hypothyroid human, although this is clearly not the case for the rat in whom hyperprolactinemia was not demonstrable. The role of VIP/PHI in human pituitary disease is unknown. We have been unable to identify any tumors that contain immunoreactive material using tissues prepared by standard methods. It may be that the demonstration of VIP/PHI is more demanding and will require better techniques for staining. The role of tuberoinfundibular VIP hypersecretion remains to be established but the evidence for stress-induced PRL hypersecretion in man encourages us to believe that at least some cases may be due to excessive hypothalamic activity. Additional potential neuroendocrine actions of VIP are in the secretomotor control of the ovary and thyroid, and in the regulation of somatostatin secretion and synthesis. In dispersed cell cultures (but not in whole hypothalamic slices from adult animals), VIP stimulates somatostatin secretion and independently stimulates the formation of somatostatin mRNA, an effect that can be duplicated in mixed cultures by treatment with forskolin, a postreceptor cAMP stimulator. In work carried out by Montminy and colleagues, the cAMP action has shown to be mediated by formation of a soluble protein that appears to activate the somatostatin gene promotor through interaction with a specific gene sequence.

Animals↗
PubMed1988

The dexamethasone suppression index: enhancement of DST diagnostic utility for depression by expressing serum cortisol as a function of serum dexamethasone.

The authors sought to determine whether the performance of the dexamethasone suppression test (DST) could be enhanced by expressing cortisol as a function of dexamethasone. Because cortisol concentration is a function of the reciprocal of dexamethasone concentration, this relationship was approximated by calculating the product of cortisol and dexamethasone as a dexamethasone suppression index. Preliminary assessment of test performance measures (sensitivity, specificity, and predictive power) showed that use of the dexamethasone suppression index was an improvement over the use of cortisol levels alone. Factoring dexamethasone levels into post-dexamethasone cortisol level measures may enhance the utility of neuroendocrine assessment in psychiatry.

Adult↗
PubMed1987

Growth hormone and prolactin responses to bolus and sustained infusions of GRH-1-40-OH in man.

To determine whether GRH stimulates PRL secretion we studied the effects of iv bolus injections and prolonged infusions of GRH 1-40-OH on PRL and GH serum levels in normal volunteers. Eight patients with acromegaly, two of whom had elevated basal levels of PRL, were also tested with single bolus injections. Six normal subjects given 3.3 micrograms/kg bolus injections of GRH showed a mean increment of GH of 22.0 +/- 1.7 ng/ml (mean +/- SE). A small rise in PRL was noted in 5 of the 6 subjects (mean peak level of 6.4 +/- 1.9 ng/ml vs basal level of 3.3 +/- 0.4 ng/ml, p less than 0.05). During the continuous intusion of GRH (10 ng/kg/min), GH levels rose gradually from a mean baseline of 1.1 +/- 0.1 ng/ml to a mean peak of 30.0 +/- 7.2 ng/ml at about 2 h and then slowly declined to a nadir of 4.2 +/- 0.4 ng/ml at 330 min. PRL levels did not rise significantly during the infusion. To determine whether the decline in GH levels in the face of continued infusion was due to loss of GH responsiveness, a 3.3 micrograms/kg bolus of GRH was given during the nadir at 330 min; this GH increment was significantly less than that obtained by the GRH bolus injection without the infusion (12.9 +/- 3.5 ng/ml vs 22.0 +/- 1.7 ng/ml, p less than 0.05). The PRL response to the GRH bolus was the same during the infusion of GRH as before. In each of 8 acromegalic patients (including two who had initially elevated basal PRL levels) GRH led to an increase in both GH and PRL levels. PRL and GH levels spontaneously fluctuated in parallel in 4 acromegalic cases studied with repeated samples over 6 h during placebo administration. These experiments show that GRH has significant, though weak, PRF effect in normals and that it is more potent PRF in acromegalic patients. Furthermore, the effects on GH and PRL of a sustained infusion of GRH for 5 1/2 h are both qualitatively and quantitatively different. These results suggest that the GRH effect is exerted either on different pituitary receptors for GH and PRL regulation, or that the releasable pools of the two hormones have different sizes and/or turnover times.

Acromegaly↗
PubMed1987

Paraventricular nucleus mediates prolactin secretory responses to restraint stress, ether stress, and 5-hydroxy-L-tryptophan injection in the rat.

The role of the paraventricular nucleus (PVN) in mediating acute stimulatory PRL responses was investigated in conscious male rats. Electrolytic lesions, verified histologically at autopsy, were stereotaxically made in the PVN region, and sham lesions were made in control rats. Blood was obtained through a chronically indwelling catheter in the right atrium. PVN-lesioned (PVL) rats showed significantly lower T3 levels 1 week after surgery (less than 34.4 ng/dl) compared with sham (mean +/- SEM, 91.2 +/- 5.0 ng/dl) and intact (86.8 +/- 2.0 ng/dl) animals, verifying a lesion in the PVN. T3 was restored to normal (95.6 +/- 1.8 ng/dl) by daily sc administration of T4 (10 micrograms/kg BW) for at least 4 days before the day of the experiments. Basal PRL levels in PVL rats did not differ significantly from those in control or sham-lesioned animals. In response to restraint stress, plasma PRL levels of PVL rats did not rise, in contrast to marked elevation in PRL in sham and intact rats [PRL levels (mean +/- SEM; nanograms per ml), basal to peak: PVL, 4.3 +/- 0.3 to 4.5 +/- 0.4; sham, 4.5 +/- 0.5 to 47.0 +/- 4.1; intact, 4.0 +/- 0.3 to 46.3 +/- 4.9]. PVL also resulted in the complete inhibition of PRL secretion induced by 30-min inhalation of ether (basal to peak: PVL, 3.3 +/- 0.3 to 4.5 +/- 0.2; sham, 5.7 +/- 0.8 to 19.9 +/- 0.9; intact, 3.3 +/- 0.4 to 27.9 +/- 4.0). The stimulatory effect on plasma PRL in sham and intact rats by one iv bolus injection of the serotonin precursor 5-hydroxy-L-tryptophan (5-HTP; 10 mg/kg BW) was completely abolished in PVL animals (basal to peak: PVL, 3.7 +/- 0.6 to 5.2 +/- 1.4; sham, 6.7 +/- 0.6 to 36.0 +/- 0.5; intact, 4.1 +/- 1.2 to 33.3 +/- 3.2). In contrast to the marked alteration in PRL regulation, PVL rats exhibited a typical ultradian rhythm of plasma GH secretion during a 6-h observation period and increased release of GH induced by iv injection of 5-HTP [GH (nanograms per ml), basal to peak; PVL, 4.5 +/- 0.6 to 21.0 +/- 4.9; sham, 3.7 +/- 0.3 to 18.4 +/- 4.4; intact, 2.9 +/- 0.1 to 17.8 +/- 3.5]. These findings indicate that PRL responses to stress and to serotonin act through the PVN, the site of origin of several putative PRL-releasing factors.(ABSTRACT TRUNCATED AT 400 WORDS)

5-Hydroxytryptophan↗
PubMed1987

Specific receptors for alpha-melanocyte-stimulating hormone are widely distributed in tissues of rodents.

alpha MSH is known to act on several nonmelanocyte cell types, which has led to recent interest in its regulatory roles in fever, inflammation, immunity, and behavior. To determine its possible sites of action, we examined the distribution of alpha MSH receptors in a variety of tissues in mice and rats. The superpotent and enzymatically resistant alpha MSH analog, Nle4,D-Phe7-alpha MSH (NDP-MSH), was radioiodinated using lactoperoxidase (Enzymobeads) and purified by reverse phase chromatography for use as a tracer. [125I]NDP-MSH exhibited consistent and specific binding to cultured B16 and Cloudman S91 murine melanoma cells, which are highly responsive to alpha MSH. The tracer had full biological activity, as determined by its potency in stimulating melanogenesis in B16 cells. To study receptor distribution in vivo, [125I]NDP-MSH was administered iv to C3H/HeJ (pigmented) mice and Sprague-Dawley (albino) rats. To determine the specificity of tracer uptake by tissues, some animals received a large molar excess of alpha MSH together with [125I]NDP-MSH. Data were expressed as tissue to plasma radioactivity concentration ratios. In mice, specific (i.e. alpha MSH-inhibitable) binding of [125I]NDP-MSH was found in a number of glandular organs, including lacrimal, Harderian, preputial, submandibular, and adrenal glands and pancreas, as well as in brown and white adipose tissues, bladder, duodenum, skin, spleen, and hypothalamus. In rats, results were generally similar; specific tracer uptake was observed in lacrimal, Harderian, preputial, and thyroid glands; pancreas, duodenum, spleen, hypothalamus; and white adipose tissue. These results show that specific receptors for alpha MSH are widely distributed, suggesting that alpha MSH may affect the functions of a number of organs.

Animals↗
PubMed1987

Pharmacokinetic studies of highly purified human prolactin in normal human subjects.

Previous estimates of PRL pharmacokinetics have been made using radioiodinated human PRL (hPRL) infusions or by measuring serum PRL disappearance following prolactinoma resection. The recent purification of hPRL in significant quantities made it possible to measure the clearance and volume of distribution directly. Studies were also carried out to determine absorption and clearance after im injection. In five normal men whose endogenous PRL secretion was suppressed by dopamine, a loading dose of hPRL (70-90 micrograms) followed by a constant infusion (1.39-2.9 ng/min) produced steady state serum PRL levels of 15.2-25.4 ng/mL by 30-60 min. The calculated mean volume of distribution was 7.3 +/- 2.9 (+/- SD) L. The calculated MCR was 71 +/- 19 mL/min X m2, and the calculated production rate was 802 +/- 377 micrograms/24 h X m2. The plasma disappearance half-life following discontinuation of the infusion was 37 +/- 10 min. The PRL infusate consisted primarily (75.6%) of a 22.5 K dalton species, probably PRL monomer, a component eluting at 45K daltons (16.1% of the total radioimmunoreactivity), probably dimer, and a small amount of a larger mol wt species. Serum obtained during dopamine infusion but before hPRL infusion contained 68.1% of the 22.5K, 7.2% of the 45K, and 24.7% of the larger mol wt moieties. During hPRL infusion in two men there was a relative decrease in the proportion of PRL monomer to 55% and 69% and a relative increase in the PRL dimer to 33% and 18%, respectively. hPRL was injected im in doses of 1, 2, 4, and 8 micrograms/kg without prior dopamine infusion. No significant changes in serum PRL levels occurred after the 1 and 2 micrograms/kg doses (n = 5). After the 4 micrograms/kg dose (n = 8), mean serum PRL levels rose from 10.0 +/- 1.8 (+/- SEM) ng/mL to peak levels of 13.1 +/- 1.8 ng/mL (P less than 0.01). After the 8 micrograms/kg dose (n = 7), PRL levels rose from 9.3 +/- 1.6 to 16.5 +/- 1.8 ng/mL (P less than 0.01). The PRL rise began between 60 and 80 min after injection; peak levels occurred at 160-180 min. In two men given 8 micrograms/kg who were sampled for an additional 3 h, PRL levels peaked at 200-220 min and began to fall by 220-240 min, but had not returned to baseline by 6 h. There were no side-effects of PRL administration, although the 8 micrograms/kg dose caused transient local discomfort.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1987

Secretion of somatostatin and its physiologic function.

Somatostatin, initially described as a growth hormone release-inhibitory peptide 14 amino acids in length, has been shown to be one of a family of related peptides. It is ubiquitous in distribution and versatile as a paracrine factor with a potentially important role in the regulation of gut, pancreatic, and nervous system function in addition to its well-recognized influence on the pituitary secretion of growth hormone and thyroid-stimulating hormone. With the development of new super agonists, it has become possible to manipulate the endocrine milieu, to modify gut, pancreatic, and pituitary function, and in the case of several diseases such as acromegaly, intractable diarrhea, and carcinoid, to make a significant advance in therapy.

Animals↗