Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Short term (30 min) infusion of cyclic somatostatin (50 microgram/rat), insulin (1 U/rat) or the two together significantly suppressed urinary cyclic AMP excretion in streptozotocin-diabetic rats. While somatostatin tended to increase cyclic GMP excretion, insulin had an opposite effect in diabetic but not in normal rats. It is suggested that somatostatin suppresses cyclic AMP excretion by inhibiting directly adenylate cyclase in liver and perhaps in other organs. The possibility that suppression of urinary cyclic AMP is due to inhibition of glucagon secretion is also considered.
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PMID:Somatostatin inhibits urinary cyclic AMP excretion in diabetic rats. 19 95

Hyperglycemia, hyperglucagonemia and hyperinsulinemia were observed in fasting rats at 0.5 hr after ip injection of NiCl2 (68 mumole per kg). Infusion of somatostatin iv (0.5 mg per rat) did not prevent Ni(II)-mediated hyperglycemia, hyperglucagonemia or hyperinsulinemia. Exposure of rats to inhalation of Ni(CO)4 (1.2 to 6.4 mumole per liter of air per 15 min) caused acute hyperglycemia, similar to that observed after ip injection of NiCl2. Hyperglycemia induced by NiCl2 and Ni(CO)4 was not associated with inhibition of erythrocyte glycolysis measured in vitro by erythrocyte uptake of 1-14C-glucose and release of 14CO2. These findings indicate that Ni-induced hyperglycemia may be mediated by increased pancreatic release of glucagon, but that Ni stimulation of glucagon release differs from stimulation of glucagon release by arginine or epinephrine, since the Ni effect is not antagonized by somatostatin.
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PMID:Effects of nickel chloride and nickel carbonyl upon glucose metabolism in rats. 73 12

We studied the effect of histamine on serum prolactin and thyrotropin (TSH) levels in male rats with anterolateral hypothalamic deafferentation of hypothalamic connections or anterolateral cut (ALC). The success of ALC was confirmed by immunohistochemistry of somatostatin (SRIF) in the medial basal hypothalamus. ALC did not affect basal prolactin or TSH levels. Thyrotropin-releasing hormone (TRH, 200 ng/rat, i.p.) did not affect prolactin secretion either in sham-operated or ALC rats. In sham-operated rats intracerebroventricularly administered histamine increased significantly prolactin levels. Hypothalamic deafferentation abolished the effect of histamine on prolactin levels. TRH increased significantly serum TSH levels both in sham-operated controls and ALC rats. In the latter, however, the TSH-secretory response to TRH was significantly (p less than 0.05) larger compared to the controls. Intracerebroventricularly infused histamine (2 micrograms/rat) did not change the TRH-induced TSH secretion in either group of rats. These results show that (1) the effect of histamine on prolactin secretion is mediated through nerve tracts which are destroyed by ALC, and (2) cutting of afferent TRH (through sensitization) and SRIF fibers (through lacking inhibition) entering medial basal hypothalamus may both contribute to the enhanced TSH response to exogenous TRH.
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PMID:Anterolateral hypothalamic deafferentation inhibits histamine-induced prolactin secretion and potentiates TRH-induced thyrotropin secretion in male rats. 194 13

In vitro degradation of 125I-labeled somatostatin-14 (Tyr11) [I-SS-14(Tyr11)] by luminal flushings of rat gastrointestinal segments was studied to characterize the fate of somatostatin in the gastrointestinal lumen. In addition, we evaluated the effect of rat milk as a potential inhibitor of luminal degradation of 125I-SS-14(Tyr11). Degradation of 125I-SS-14(Tyr11) was not detected in stomach flushings from either suckling or weanling rats. Luminal flushings from the small intestine degraded 125I-SS-14(Tyr11), with a gradient increase of activity from duodenum to midjejunum (degradation in suckling rat midjejunum and ileum was about five times lower than that in weanling rat). Degradation of 125I-SS-14(Tyr11) by luminal flushings of suckling rat midjejunum was dose dependently inhibited by rat milk casein and soluble fractions. Inhibitory activity of rat milk soluble fraction was heat labile and several times more potent than that of casein fraction. Casein fraction appeared to be stable at 100 degrees C for up to 30 min of exposure. These studies suggest that somatostatin is stable in the gastric lumen and that milk protects somatostatin from intestinal luminal proteolysis, indicating a possible physiological significance of milk-borne SS-14 for the suckling rat gastrointestinal tract.
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PMID:Inhibition of intestinal degradation of somatostatin by rat milk. 196 33

The effects of lesion of the hypothalamic paraventricular nuclei (PVNx), the main thyrotrophic area, on the cold-stimulated thyrotropin (TSH) responses to intracerebroventricular (i.c.v.) 5-HT were studied in male rats. PVNx significantly attentuated the cold-stimulated TSH levels, but significantly affected neither hypothalamic thyrotropin-releasing hormone nor somatostatin content. Serum T3 levels were significantly decreased 8 days after PVNx. Irrespective of the lesion (sham or PVNx), 5-HT infusion (9 micrograms per rat) into the posterior third ventricle attenuated markedly the cold-stimulated TSH levels, whereas infusion into the anterior third ventricle did not. Bilateral 5-HT infusions (2 micrograms per side) into the hypothalamic dorsomedial nuclei significantly decreased serum TSH, but bilateral infusions into the posterior hypothalamic nuclei were without effect. Sham-lesion and PVNx decreased serum prolactin levels without affecting the stimulation of prolactin secretion by i.c.v. 5-HT. These results suggest that the inhibitory effect of i.c.v. 5-HT on TSH secretion and its stimulatory action on prolactin secretion are only partially dependent on the PVN.
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PMID:Effects of hypothalamic paraventricular nucleus lesion on the cold-stimulated TSH responses to 5-HT in male rats. 197 6

Administration of monosodium glutamate (MSG) to neonatal rodents produces permanent lesions of hypothalamic arcuate neurons that secrete GH-releasing hormone (GHRH). The present study was intended to determine the consequences of GHRH deficiency on the pulsatile GH secretory pattern and growth in MSG-treated female rats and to compare these effects with those observed in male littermates. Male and female rats were injected with MSG [4 mg/g body wt (BW), sc] or saline (controls) on days 2, 4, 6, 8, and 10 after birth. Immunoreactive GHRH concentrations were decreased in the hypothalamus (by 60%) and in the median eminence (by 95%) of adult male and female MSG-treated rats. In contrast, somatostatin concentrations were unaffected. BW and linear growth were severely impaired in male MSG-treated rats, but in MSG-lesioned females BW was not different from controls, and the attenuation of longitudinal growth was less severe and the obesity more pronounced than in males. These sex differences occurred despite similar reductions (by 55%) in serum insulin-like growth factor I concentrations in male and female MSG-treated rats. MSG treatment also produced decreases in pituitary wt and GH content (by 60%), independent of sex. Pulsatile GH secretion was studied by serial blood sampling of chronically cannulated, freely moving rats. Plasma GH patterns were analyzed by the PULSAR program. Compared to controls, treatment with MSG led to a marked inhibition (by 90%) of GH secretion in both sexes. Significant reductions in GH pulse amplitude (-95%) and pulse duration (-62%) were observed in males, whereas pulse amplitude (-85%), pulse frequency (-67%), and baseline GH concentrations (-80%) were markedly reduced in females. The GH responses to an iv bolus injection of rat GHRH (1 microgram/rat) was severely blunted in both male and female MSG-treated rats. This study demonstrates that GHRH deficiency in female rats results in a marked inhibition of GH pulses, as in males, but also causes severe and sex-specific reductions in GH basal secretion and pulse frequency. These observations suggest that hypothalamic GHRH secretion in female rats is more continuous than in males and is a determinant of the elevated interpulse secretion of GH. Moreover, body wt and linear growth are less severely affected by arcuate lesions in female animals, compared to males. These sex-related differences in growth rates may result in part from the tendency of female MSG-lesioned rats to become more obese than males, and the development of obesity, in turn, may antagonize the factors that tend to slow linear growth.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neonatal treatment with monosodium glutamate: effects of prolonged growth hormone (GH)-releasing hormone deficiency on pulsatile GH secretion and growth in female rats. 198 48

Intracerebroventricular administration of SMS 201-995 (5 micrograms/rat), a somatostatin analogue, induced barrel rotation in rats. Pretreatment with ceruletide (40 micrograms/100 g b. wt., IP) 3 days or 7 days prior to the injection of SMS 201-995 significantly inhibited the response rate of barrel rotation induced by SMS 201-995, but not that induced by arginine-vasopressin (1 microgram/rat, ICV). The suppressive effect of ceruletide on barrel rotation could be partially countered by MK-329, a selective peripheral CCK (CCK-A) receptor antagonist. Desulfated cerulein did not affect the barrel rotation induced by SMS 201-995. These findings suggest that ceruletide specifically suppresses the barrel rotation evoked by SMS 201-995 in a long-lasting manner possibly acting through CCK-A receptor.
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PMID:Barrel rotation in rats induced by SMS 201-995: suppression by ceruletide. 208 92

The effects of central 5-hydroxytryptamine (5-HT) infusions on the cold-stimulated thyrotropin (TSH) levels were studied in male rats. Stainless-steel cannulas were implanted stereotaxically into the anterior or the posterior third ventricle or just lateral to the hypothalamic paraventricular nuclei bilaterally 7 days before experiments. Infusion of 5-HT (4.5 and 9 micrograms/rat) into the posterior third ventricle attenuated significantly the cold-stimulated TSH levels. Inversely, infusion of 5-HT (9 micrograms/rat) into the anterior third ventricle augmented significantly the TSH cold response. Bilateral 5-HT infusions into the vicinity of the hypothalamic paraventricular nuclei did not affect the TSH cold response. Serum prolactin levels increased significantly after 5-HT administration into the anterior and the posterior third ventricle, but no consistent effect on growth hormone (GH) levels could be detected. Infusion of 5-HT into the anterior and the posterior third ventricle decreased body temperature irrespective of the observed hormonal response to 5-HT. The results are in favor of a dual and possibly site-dependent role for 5-HT in the regulation of the cold-stimulated TSH secretion in the rat. The opposite effects of 5-HT on the TSH cold response may result from the predominant inhibition of either the thyrotropin-releasing hormone or the somatostatin-secreting cell groups.
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PMID:Site-dependent action of intracerebroventricular 5-hydroxytryptamine on the cold-stimulated thyrotropin secretion in male rats. 210 86

Peptide-containing nerve fibers were found to be numerous in the glandular stomach of the rat and mouse. The immunoreactive neuropeptides demonstrated included vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine (PHI), gastrin-releasing peptide (GRP), substance P (SP), enkephalin, somatostatin, cholecystokinin, and neuropeptide Y (NPY). The density and distribution of the various peptide-containing fibers did not differ overtly between the pyloric and oxyntic gland areas except for the GRP fibers, which were fewer in the pyloric than in the oxyntic mucosa. The entire VIP nerve fiber population was found to also contain PHI. Immunoreactive NPY was found to occur in the VIP/PHI fibers (VIP/PHI/NPY fibers) in the smooth muscle and intramural ganglia of both rat and mouse and in the mucosa of the mouse. Mucosal VIP/PHI fibers in the rat did not contain any NPY-like material. Perivascular NPY fibers in both species and mucosal NPY fibers in the rat did not contain VIP or PHI. The mucosa harbored numerous GRP fibers and VIP/PHI (rat) or VIP/PHI/NPY (mouse) fibers, and a modest number of NPY (rat) and SP fibers. In the submucosa the peptide-containing nerve fibers were found mainly in the ganglia and around blood vessels. Blood vessels received a rich supply of NPY fibers; the number of perivascular VIP/PHI, GRP, and SP fibers was much lower by comparison. The smooth muscle and myenteric ganglia harbored not only VIP/PHI/NPY, GRP, and SP fibers but also enkephalin, somatostatin, and cholecystokinin fibers. Gastrin-releasing peptide, VIP/PHI/NPY, SP, and enkephalin nerve cell bodies occurred in the myenteric ganglia. As studied in the rat, vagal denervation did not affect the density and distribution of the various peptide-containing nerve fibers. After sympathectomy, mucosal and perivascular NPY fibers disappeared. The other types of peptide-containing nerve fibers were not affected.
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PMID:Peptide-containing nerve fibers in the stomach wall of rat and mouse. 240 58

The developmental patterns of neurofilament triplet proteins, peptide and amine immunoreactivities were compared in motor (ventral spinal cord), sensory (dorsal spinal cord, dorsal root ganglia, epidermis), and autonomic (intermediolateral cell columns, dermis) regions in the rat and human. In the rat, neurofilament triplet proteins first appeared in motoneurones (embryonic day 13). In the youngest human fetuses studied (6 weeks), immunoreactivity was present throughout the spinal cord. Peptides and amines occurred later. Calcitonin gene-related peptide, galanin, somatostatin, neuropeptide Y and its C-flanking peptide (CPON) were the first to appear localized to motoneurones (embryonic days 15-17 rat; fetal weeks 6-14 human). Numbers of immunoreactive motoneurones decreased toward birth, but immunoreactive fibers increased in the ventral horn with enkephalin, thyrotrophin-releasing hormone, and the monoaminergic markers 5-hydroxytryptamine and tyrosine hydroxylase (all presumably of supraspinal origin) the last to appear perinatally. In the dorsal horn, particularly in the rat, a transient expression of substance P-, somatostatin-, and neuropeptide Y/CPON-immunoreactive cells was detected (embryonic days 15-17). A pronounced increase of calcitonin gene-related peptide-, galanin-, somatostatin- and substance P- immunoreactive fibers was found perinatally in both species. This coincided with an increased detection of cells in the dorsal root ganglia containing these peptides and the earliest appearance of calcitonin gene-related peptide-, somatostatin-, and substance P-immunoreactive fibers in the rat epidermis. Few antigens were localized to the intermediolateral cell columns before embryonic day 20 (rat), fetal week 20 (human), with thyrotrophin-releasing hormone-, 5-hydroxytryptamine-, tyrosine hydroxylase-, and vasoactive intestinal polypeptide-immunoreactive nerves appearing perinatally. In the rat dermis, tyrosine hydroxylase-immunoreactive fibers (sympathetic fibers) and fibers immunoreactive for neuropeptide Y/CPON and vasoactive intestinal polypeptide were detected from postnatal day 1. In conclusion, 1) peptide and amine immunoreactivity develops in motor before sensory or autonomic regions, 2) many peptide-containing cells are transient in fetal life, and 3) central terminals of dorsal root ganglion cells express peptides before terminals in the skin.
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PMID:Ontogeny of peptide- and amine-containing neurones in motor, sensory, and autonomic regions of rat and human spinal cord, dorsal root ganglia, and rat skin. 244 34


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