UNIPROT:P61278 - FACTA Search

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Query: UNIPROT:P61278 (somatostatin)
22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growth hormone (GH) release is influenced mainly by two hypothalamic factors, growth hormone-releasing factor (GRF) and somatostatin and is modulated by other hormones such as gonadal steroids. The objective of this study was to determine if castration (CA) and exogenous testosterone (TE) affect endogenous and GRF-induced GH release. Purebred Yorkshire male pigs (n = 32) were assigned to one of the following treatments: T1:CA; T2:CA +/- TE; T3: intact (IN); T4: IN +/- TE, in a 2 x 2 factorial design. Piglets were castrated at 3 days of age. Testosterone propionate (1.0 mg/kg) in sesame oil (2 ml) or sesame oil alone was injected sc SID during a 10-day period before each sampling day at 9, 15 and 21 weeks of age. Jugular blood samples were collected for a 6-hr period preceding and following iv injection of hGRF (1-29)NH2 (10 micrograms/kg). These procedures were repeated at 9, 15 and 21 weeks of age. The overall mean GH levels and the area under the GH peaks before and after GRF stimulation were lower (P less than .05) in castrated animals than in intact animals. Testosterone treatment increased (P less than .05) circulating TE levels and increased the amplitude of the endogenous GH peaks but did not affect (P greater than .05) the GRF-induced GH release. Increasing age produced a marked reduction of the amplitude of the GH peaks, the area under the GH peaks, the baseline mean and the overall mean GH levels during the 6-hr period preceding GRF injection. The present data support the hypothesis that castration in pigs reduces circulating and GRF-induced GH release. Exogenous testosterone for 10 days did not stimulate endogenous or GRF-induced GH release with the exception of the amplitude of the endogenous GH peaks.
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PMID:Castration and testosterone effects on endogenous and somatocrinin-induced growth hormone release in intact and castrated male pigs. 249 17

In the male rat, GH secretion is characterized by high amplitude pulses that appear at regular intervals of 3-4 h, with low basal levels between such pulses. In the female, the pulses are irregular and more frequent, with lower amplitudes, while basal secretion is higher. The present study was designed to exclude the indirect effects of sex steroids on the pituitary, enabling investigation of the direct effects of sex steroids on the pituitary. Rats were gonadectomized at 22 days of age, and 12 days later their anterior pituitaries were trypsinized for cell dispersion. Testosterone (T) or 17 beta-estradiol (E2), 5 nM, was added to the medium for 6 days, and subsequently, GRF or somatostatin was added for 4 h. In a perifusion system, the male-derived cell response to GRF was augmented after pretreatment with T, but not with E2. The female-derived cell response to GRF was augmented by E2, but not by T. T increased the sensitivity of the cells to GRF from 3.0-0.03 nM and increased the maximal potency of GH secretion 3-fold. E2 had no significant effect on the sensitivity, but lowered the potency. Somatostatin (1 nM) inhibited GH secretion by 44% in T-treated cells. In E2-treated cells, somatostatin was ineffective. GRF increased the total amount of GH (medium plus cells) in both T- and E2-treated cells, but not in control pituitary cells. It is suggested that T has direct effects on the male somatotroph. By increasing the pituitary cell responses to GRF and somatostatin, T contributes to the high amplitude peak/low baseline pattern of the male. By decreasing the pituitary cell responses to GRF and somatostatin, E2 contributes to the low amplitude peak/high baseline pattern of the female.
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PMID:Effects of sex steroids on the response of cultured rat pituitary cells to growth hormone-releasing hormone and somatostatin. 256 24

The modulatory effects of glucocorticoid and sex steroid hormones on the effects of rat GH-releasing factor (GRF) and somatostatin (SRIF) on GH release and biosynthesis were studied in monolayer cultures of rat anterior pituitary cells with RIA and quantitative immunoprecipitation methods. Dexamethasone (10(-7) M), a potent synthetic glucocorticoid, increased both the sensitivity and maximum response of GH release stimulated by GRF. Progesterone (10(-7) M) also enhanced GH release stimulated by GRF. The stimulatory effects of dexamethasone and progesterone were dose dependent and required a latent period of at least 24 h to be evident. Testosterone, dihydrotestosterone, and 17 beta-estradiol showed no apparent influence on GRF-induced GH release under the same conditions. None of the hormones studied showed significant influences on basal or SRIF-suppressed GH release. Progesterone added to the maximally effective concentrations of dexamethasone had no additional effects on GRF-induced GH release. The effect of progesterone was attenuated by both 5 alpha-dihydronorethindrone, a progesterone antagonist and 17 alpha-methyltestosterone, a glucocorticoid antagonist. In terms of GH synthesis, stimulatory effects of GRF on GH synthesis were apparent only when pituitary cells were pretreated with dexamethasone. These results indicate that: pretreatment with glucocorticoid or progesterone enhances the effects of GRF on GH release and/or synthesis; these two steroids share at least one common step to enhance GRF effects; and steroid hormones have little influence on basal or SRIF-suppressed GH release.
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PMID:Influence of sex steroid hormones on rat growth hormone-releasing factor and somatostatin in dispersed pituitary cells. 287 86

Harderian glands of Syrian hamsters contained measurable levels of immunoreactive somatostatin. After an extraction procedure, serial dilutions of tissue were assayed and showed parallelism in the displacement curve with dilutions of purified somatostatin standard in the radioimmunoassay. Somatostatin concentrations were higher in female hamsters (10.0 +/- 2.1 ng/mg protein) than in males (2.6 +/- 0.4 ng/mg protein). Castrated males had somatostatin values in the range of females (12.4 +/- 2.3 ng/mg protein) at 1 month after gonadectomy. Testosterone implants prevented the rise of Harderian gland somatostatin in castrated males. Gonadectomized males had lower somatostatin content in the gland than did control males (1.0 +/- 0.2 ng/mg protein) at 2 months after castration. Somatostatin values in females were unaffected by gonadectomy, but there were variations during the oestrous cycle, with a nadir detected at dioestrus-1 and maximal values coincident with the day of the ovulation.
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PMID:Androgenic control of immunoreactive somatostatin in the Harderian gland of the Syrian hamster. 289 44

To investigate whether the effects of testosterone (T) on endosteal bone metabolism may be mediated by growth hormone (GH), intact male mice were infused for ten days with T (5 or 15 mg/kg/d) alone, or combined either with native somatostatin (SRIF) (220 micrograms/kg/d) or with the long-acting somatostatin analog SMS 201-995. Testosterone infusion induced a dose-dependent increase in histomorphometric parameters of bone formation, causing a 25% increase in osteoblastic and osteoid surface and 10% to 12% stimulation of the matrix and mineral appositional rates. Stimulation of bone formation rate was associated with a 2- to 3-fold increase in the incidence of serum GH peaks of high amplitude. SRIF (220 micrograms/kg/d) and SMS at low dose (4.32 micrograms/kg/d) decreased parameters of bone formation by 20% to 25%. At a higher dosage (13 micrograms/kg/d), which mildly decreased serum glucose and longitudinal bone growth, SMS further reduced bone formation rate. Infusion of SRIF with T (5 mg/kg/d) blunted the stimulatory effect of T. Similarly, infusion of a high dose of SMS (13 micrograms/kg/d), together with T (15 mg/kg/d), abolished the effect of T (15 mg/kg/d) without altering serum glucose or mineral levels. The effect of SRIF on testosterone-induced (5 mg/kg/d) bone formation was associated with inhibition of T-induced high-amplitude GH peaks. The results indicate that T stimulates the osteoblastic bone formation in association with increased GH secretion, whereas SRIF and the analog SMS produce inhibitory effects.
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PMID:Somatostatin infusion inhibits the stimulatory effect of testosterone on endosteal bone formation in the mouse. 289 69

In this review, we examine the changes in sexual function that accompany deviations from "normal" physiological states. We propose that the changes one observes in many altered physiological states should not be viewed in isolation. We describe our paradigms for assessing sexual function, and proceed to evaluate how sexual function changes with hormonal deprivation and aging, in rat models for hypertension, in severe hyperprolactinemia, in streptozotocin-induced diabetes, after chronic alcohol intake, after chronic morphine administration, and after exposure to the heavy metal, cadmium. We will provide evidence for the involvement of adrenergic transmitters and two neuropeptides, neuropeptide Y and somatostatin, in the neuroendocrine regulation of sexual behavior. Finally, we compare and contrast the changes observed relative to the changes seen in "normal" aging in rats. The sequence of age-related changes in sexual function is distinct. The first change observed is a decrement in ex copula erectile reflexes. Next are decreases in ejaculatory threshold, followed shortly by increases in initiation and reinitiation of copulation after ejaculation. This is followed by a decrement in the number of males copulating to ejaculation. Finally, there is a failure to initiate the copulatory process. This sequelae is relatively common, being evident after castration, with hyperprolactinemia, and after exposure to cadmium. The data available for sexual function in hypertension is incomplete and modified by the etiology, but a suggestion for this sequelae is seen in SHR. In contrast, sexual dysfunction associated with chronic morphine administration appears to be due to an initial deficit in motivational aspects. Testosterone reverses sexual dysfunction associated with castration, but not with idiopathic sexual inactivity, nor with sexual dysfunction associated with aging, diabetes, or chronic morphine administration. Comparing sexual function in rat models for hypertension, diabetes and chronic ethanol leads to the conclusion that increases in blood pressure, like decreases in testosterone, cannot be the primary causal factor for sexual dysfunction. Age, hormonal history of the subject, and the age at castration influence changes in sexual function. Age-related sexual dysfunction appears to be contributed to by changes in adrenergic-neuropeptidergic, to include sympathetic, systems. Site-specific administration of NPY induces alterations in parameters of copulatory behavior which mimic those seen in aging and the retention of ejaculatory behavior with aging is associated with site-selective attenuation (or reversal) of age-associated changes in NPY content. Yohimbine enhances copulatory activity in castrated and aging rats, and attenuates or reverses the antisexual effects of clonidine, epinephrine and somatostatin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Sexual function in altered physiological states: comparison of effects of hypertension, diabetes, hyperprolactinemia, and others to "normal" aging in male rats. 763 May 83

Testosterone (T) administration to pubertal boys increases spontaneous GH secretion. It is not known whether this occurs via pituitary or hypothalamic mechanisms. We evaluated the GH secretion of 12 boys, aged 13.67 +/- 0.37 yr (mean +/- SE), diagnosed with constitutional delay in growth and adolescence. The evaluation was made both before and after 3 months of treatment with T or the nonaromatizable androgen, 5 alpha-dihydrotetosterone. Serum for determination of spontaneous GH secretion was sampled every 20 min for 24 h. Pituitary responsiveness was assessed by the administration of GHRH with sampling of GH at intervals for the next 2 h. This was also done with pyridostigmine (PDS) pretreatment to assess the effects of somatostatin. The dose of androgen used was 80 mg/m2 month. All tests were then repeated during treatment. Spontaneous GH secretion was analyzed by the Cluster method. The response to GHRH was measured as the area under the curve. Somatostatin effects were quantified as the difference in responsiveness between the two GHRH tests performed at each admission: one without prior PDS administration and one in which somatostatin was blocked by PDS. Treatment with T increased mean spontaneous GH secretion from 2.25 +/- 0.34 micrograms/L before treatment to 6.77 +/- 0.69 micrograms/L (mean +/- SE; P < 0.001) and mean spontaneous peak height from 5.62 +/- 1.05 to 17.21 +/- 1.52 micrograms/L (mean +/- SE; P < 0.001). No significant differences between pretreatment and treatment evaluations for any spontaneous GH secretory parameters were seen in 5 alpha-dihydrotestosterone-treated patients, except that maximum peak height was decreased after treatment (P < 0.02). In T treated patients, the GHRH stimulation tests without prior PDS administration changed from 84.14 +/- 34.54 total micrograms/L before to 102.3 +/- 35.82 total micrograms/L (mean +/- SE; P = NS) after androgen treatment. PDS pretreatment produced an increase in responsiveness to GHRH over the test without PDS pretreatment. This increase was 127.03 +/- 35.68 total micrograms/L before T treatment; after T treatment, this increase was 78.38 +/- 57.6 total micrograms/L (mean +/- SE; P = NS). T treatment, via an estrogen-dependent mechanism, caused increased GH pulse amplitude, thereby increasing the mean serum GH concentration. This increase was not the result of increased pituitary responsiveness or decreased somatostatin tone. This indicates that T exerted its effect on GH via increased GHRH pulse amplitude.
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PMID:The effects of testosterone and dihydrotestosterone on hypothalamic regulation of growth hormone secretion. 877 2

Testosterone exerts important feedback effects on the hypothalamus of the ram to influence reproductive functioning. To provide a neuroanatomical basis for understanding this androgen action, the present study has examined androgen receptor (AR) immunoreactivity within the hypothalamus and adjacent brain areas of the intact non-breeding season ram. The largest populations of AR-immunoreactive cells were detected in the medial preoptic area, infundibular and premammillary nuclei in addition to the ventromedial nucleus (VMN) where cells were found distributed throughout its medial and lateral divisions. Smaller numbers of AR-expressing cells were identified in the bed nucleus of the stria terminalis and anterior hypothalamic area (AHA) including the paraventricular, but not the supraoptic, nucleus. Double-labelling immunocytochemistry revealed the presence of AR immunoreactivity in only 2 of 460 gonadotropin-releasing hormone (GnRH) neurons. A very small population of TH-immunoreactive cells located in the lateral aspect of the AHA was found to contain ARs. Dopaminergic cells elsewhere in the hypothalamus, including the infundibular nucleus, did not display AR immunoreactivity. Nearly 50% of AR-expressing cells in the lateral VMN were immunoreactive for somatostatin while less than 5% of periventricular somatostatin neurons displayed AR immunoreactivity. These results show where ARs are expressed in the ram hypothalamus and indicate the neuroanatomical sites at which androgen may act to influence reproductive function. The absence of ARs in the neuroendocrine GnRH and tuberoinfundibular dopaminergic cells suggests that androgens do not influence the genome of these cells in any direct manner. In contrast, the somatostatin neurons of the VMN appear to be an important target for circulating androgens in the non-breeding season ram.
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PMID:Androgen receptor-immunoreactive cells in ram hypothalamus: distribution and co-localization patterns with gonadotropin-releasing hormone, somatostatin and tyrosine hydroxylase. 905 76

Recently, our laboratory has identified three distinct pre-pro-somatostatin (PSS) genes in goldfish brain: PSS-I encodes for somatostatin (SRIH)-14, PSS-II encodes SRIH-28, which contains [Glu(1), Tyr(7), Gly(10)] SRIH-14 at its C-terminus, and PSS-III encodes [Pro(2)] SRIH-14. In goldfish, increasing levels of the sex steroid estradiol increase the plasma levels of growth hormone (GH). However, whether sex steroids act at the level of the brain to regulate GH release is unclear. In the present study, the effects of sex steroids on the expression of the three PSS genes in goldfish forebrain were examined. The results demonstrate that treatment with estradiol significantly increases the expression of PSS-I and PSS-III genes in both male and female fish. The effects of estradiol were evident after only 2.5 days of treatment. Testosterone treatment increased the expression of PSS-I and PSS-III genes in female but not male fish, and only at the highest dose used. In addition, the effects of testosterone were evident only after treatment for 5 or 10 days and were blocked by an aromatase inhibitor, suggesting that testosterone must be converted to estradiol to exhibit the effect. Neither estradiol nor testosterone treatment had effects on the expression of the PSS-II gene. These results suggest that sex steroids can act either directly or indirectly on the brain to regulate PSS-I and PSS-III gene expression, influencing in turn the regulation of GH secretion.
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PMID:Regulation of expression of somatostatin genes by sex steroid hormones in goldfish forebrain. 1209 12

Testosterone (T) is known to affect the growth hormone (GH) axis. However, the mechanisms underlying the activation of GH secretion by T still remain to be clarified. Available data in animals and humans have shown that withdrawal of somatostatin (SRIH) infusion induces a GH-releasing hormone (GHRH)-mediated rebound release of GH, and there is accumulating evidence that SRIH infusion withdrawal may be a useful test to probe the GHRH function in vivo. With the aim of investigating whether the stimulatory effect of androgens on GH release in man could be accounted for by activation of the hypothalamic GHRH tone, we evaluated the plasma GH response to SRIH withdrawal in 10 patients aged 29.6 +/- 2.4 years (mean +/- SEM), diagnosed with hypergonadotropic hypogonadism, before and after a 6-month replacement therapy with T enanthate (250 mg every 3 weeks, i.m.), and in 10 healthy men, aged 26.7 +/- 2.8 years. To verify whether the modulation of GH secretion by T could also be mediated through changes in SRIH tone and/or pituitary releasable pool, we examined GH secretory responses to combined GHRH and L-arginine (ARG) in the same individuals. Basal plasma concentrations of GH (0.48 +/- 0.11 microg/l) and IGF-I (23.79 +/- 1.83 nmol/l) were significantly lower in untreated hypogonadal patients than in healthy men, and significantly increased after T replacement therapy (GH 1.13 +/- 0.28 microg/l; IGF-I 28.71 +/- 1.46 nmol/l). The mean Delta GH peak after SRIH withdrawal recorded in untreated hypogonadal men (2.65 +/- 0.86 microg/l) was significantly (p < 0.05) lower than that observed in healthy men (6.53 +/- 1.33 microg/l) and significantly increased after T replacement therapy (5.52 +/- 1.25 microg/l). The GH responses to GHRH combined with ARG (a functional SRIH antagonist) were not significantly different between healthy men and untreated hypogonadal patients, and were not significantly affected by T treatment. Plasma T and estradiol (E(2)) levels significantly correlated with Delta GH peak after SRIH withdrawal in healthy men and in T-treated hypogonadal patients, whereas in untreated patients they did not. No significant correlation was found between GH areas under the curve after GHRH + ARG test and T and E(2) plasma levels in either healthy men or in hypogonadal patients (both before and after T replacement). These findings are consistent with the view that in humans the stimulatory action of T on the GH axis appears to be mediated at the hypothalamic level primarily by promoting GHRH function.
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PMID:Activation of the somatotropic axis by testosterone in adult men: evidence for a role of hypothalamic growth hormone-releasing hormone. 1284 24

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