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)

This study examined the relationship between postnatal metabolic and hormonal changes and the accompanying rapid increase in mitochondrial adenine nucleotide content (ATP + ADP + AMP) in rabbit liver. The cytosolic NAD+/NADH concentration ratio, calculated from tissue pyruvate and lactate values, increased linearly 6.6-fold during the 1st postnatal h. The mitochondrial NAD+/NADH concentration ratio, calculated from tissue acetoacetate and beta-hydroxybutyrate values, increased 28-fold by 30 min postnatal. These changes in NAD+/NADH suggest that tissue oxygenation occurs rapidly and that oxygen supply rather than substrate supply is limiting for mitochondrial respiration in the immediate postnatal period. The normal increase in mitochondrial adenine nucleotide content that occurs within 2 h after birth was inhibited by hypoxia (5% O2). Glucagon stimulated the postnatal increase in mitochondrial adenine nucleotides but had no effect in combination with hypoxia. Both glucose and somatostatin injections inhibited the increase in mitochondrial adenine nucleotides and increased the insulin-to-glucagon ratio. Isoproterenol or dibutyryl cAMP stimulated, but propranolol did not inhibit, the normal increase in mitochondrial adenine nucleotide content. Phentolamine did not stimulate the postnatal accumulation of adenine nucleotides. In summary, the results show that the insulin-to-glucagon ratio is probably the most important hormone regulator of the rapid recompartmentation of adenine nucleotides into the mitochondrial matrix and that tissue oxygenation is strictly permissive for this hormone effect in the first 2 h after birth.
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PMID:Regulation of mitochondrial adenine nucleotide content in newborn rabbit liver. 289 2

Brush border membrane vesicles (BBMV) and basolateral membrane vesicles (BLMV) were simultaneously prepared from surgically resected pieces of morphologically intact human duodenum with a modified Percoll gradient centrifugation method. Alkaline phosphatase was enriched 20-fold in BBMV, whereas (Na+ + K+)-stimulated adenosine triphosphatase was enriched 15-fold in BLMV. BBMV and BLMV were preincubated with 3 microM synthetic somatostatin-14 or 3 microM SMS 201-995 for 10 min at 5 degrees C. In BBMV calcium, sodium, D-glucose, L-alanine, and D-mannitol uptake was unaffected by somatostatin-14 and SMS 201-995. In BLMV we found two Ca++ transport systems: Na+/Ca++ exchange and ATP-driven Ca++ transport. Somatostatin-14 had no effect on either of the two transport mechanisms. SMS 201-995 had no effect on Na+/Ca++ exchange but significantly inhibited basolateral ATP-dependent Ca++ transport (-40% +/- 5%, p less than 0.005).
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PMID:Effect of the somatostatin analogue SMS 201-995 on ATP-dependent calcium transport of basolateral vesicles from human duodenum. 289 47

Studies in the effect of somatostatin and dopamine on the incorporation of 32P from ATP to casein and ribosomes were carried out using purified protein kinase type II, isolated from the human placental cytosol. Low concentrations of somatostatin inhibited, while high ones of dopamine concentrations stimulated the activity of kinase.
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PMID:Effect of somatostatin and dopamine on the activity of cyclic AMP-independent protein kinase from human placenta. 289 20

Somatostatin, an hyperglycemia-inducing hormone, was studied in rat insulinoma (RINm5F) cells using 86Rb+ efflux techniques. 86Rb+ efflux is stimulated by somatostatin in a dose-dependent manner. The half-maximum value of activation is 0.7 nM. Somatostatin-induced 86Rb+ efflux is abolished by the hypoglycemia-inducing sulfonylurea, glibenclamide, a known blocker of ATP-regulated K+ channels. Somatostatin activation is prevented by pretreatment of insulinoma cells with pertussis toxin. 86Rb+ efflux studies show that somatostatin activates an ATP-dependent K+ channel.
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PMID:Somatostatin activates glibenclamide-sensitive and ATP-regulated K+ channels in insulinoma cells via a G-protein. 290 89

The present study was undertaken to investigate the acute and long-term effects of streptozotocin (SZ) on pancreatic islet function and survival in vitro. Isolated mouse pancreatic islets, that had been cultured overnight, were exposed to SZ (0.55-4.4 mM) or critic acid buffer in the case of the control group. The islets were examined either immediately after SZ exposure or after one week in culture. There was a marked loss of islets treated with 2.2 and 4.4 mM SZ during the culture; however, the DNA content of the remaining islets was unaffected. The islet insulin content was reduced 7 days after treatment with 2.2 and 4.4 mM SZ. At 4.4 mM the glucagon and somatostatin content of the islet was also decreased but not to the same degree as the insulin content. SZ-induced inhibition of glucose-stimulated insulin release and (pro)insulin biosynthesis was more pronounced on day 7 as compared to day 0. A similar pattern of inhibitory action of SZ was observed on islet glucose oxidation rates. Islet ATP contents were depressed on day 7 in islets exposed 4.4 mM SZ, but were otherwise similar to the control group. Islet NAD + NADH contents were decreased by 50% after exposure to 2.2 mM SZ, compared to the control islets on day 0. This decrease in NAD + NADH contents was to a large extent restored during the one-week culture. The present study shows that islets failed to completely repair the acute damage caused by SZ, and that the impairment of the islet glucose-stimulated insulin release induced by SZ seemed to progress in culture.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Functional characteristics of cultured mouse pancreatic islets following exposure to different streptozotocin concentrations. 297 3

Isolated rat pancreatic islets, incubated in the presence of extracellular 32Pi to a state of steady 32P incorporation into cellular phosphopeptides, were exposed to glucagon, (Bu)2cAMP, or somatostatin for 10 min. In other experiments, homogenates of rat islets were phosphorylated using [gamma-32P]ATP with or without cAMP. Proteins were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and phosphorylation of proteins was measured by liquid scintillation counting of gel slices. Glucagon (2.9 X 10(-7) M) stimulated the phosphorylation of 15 polypeptides (by approximately 20-50%) with major phosphorylation of proteins with mol wts of 138,000, 93,000, 53,000, 49,000, 35,000, 27,000 and 15,000 in intact rat islets and also stimulated insulin release by 202%. Somatostatin (6.6 X 10(-7) M) inhibited all the glucagon-stimulated phosphorylation by approximately 15-30% and also inhibited the glucagon-stimulated insulin release by 46%. (Bu)2cAMP (10(-3) M) stimulated 32P incorporation (by approximately 20-50%) into the same 15 peptides as did glucagon and also stimulated insulin release by 169%. When homogenates of rat islets were used. cAMP (10(-6) M) stimulated the phosphorylation of proteins (by approximately 25-60%) to an extent similar to that seen in the presence of glucagon or (Bu)2cAMP in intact islets. These findings indicate that the glucagon-stimulated phosphorylation of rat islet proteins may be mediated by cAMP-dependent protein kinase and that protein phosphorylation may be important in mediating the glucagon-stimulated insulin release.
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PMID:Effect of glucagon and cyclic adenosine 3',5'-monophosphate on protein phosphorylation in rat pancreatic islets. 612 26

Specific [125I]-Iodo-NTyr somatostatin binding sites are present in adenohypophyseal and cerebral cortical membranes. Guanine nucleotides reduce the maximal binding capacity of adenohypophyseal binding sites without significantly affecting their apparent affinity. In pituitary as well as in cortex, GTP is the most potent nucleotide followed by GDP and guanylyl imidodiphosphate (GMP-PNP). The effect appears specific of guanine nucleotides since ATP, ADP and AMP are inactive on [125I]-Iodo-NTyr somatostatin binding. These results, showing the nucleotide sensitivity of [125I]-Iodo-NTyr somatostatin binding in pituitary and cerebral cortex, are compatible with a coupling of somatostatin receptors with adenylate cyclase.
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PMID:Guanine nucleotide sensitivity of [125I]-Iodo NTyr somatostatin binding in rat adenohypophysis and cerebral cortex. 613 1

Secretion of chloride from blood to lumen is accomplished in the rectal gland of elasmobranchs by a process of secondary active transport involving the co-transport of Cl- with Na+ across the basolateral membranes of rectal gland cells. Energy is provided by ATP via membrane Na-K-ATPase, which establishes an electrochemical gradient favouring Na+ influx into the cell. The involvement of K+ in the co-transport mechanism, so as to provide a ratio of 1 Na+:1 K+:2 Cl- entering the cell, would increase the energetic efficiency of the process, and is consistent with the Cl/O2 ration of 27-30 observed in secreting rectal glands. Secretion is stimulated by cyclic AMP (cAMP) and by vasoactive intestinal peptide (VIP) and adenosine, which activate adenylate cyclase. Activation of the gland in vivo probably occurs via VIP-secreting nerves as well as circulating agents; it is inhibited by somatostatin. Cyclic AMP probably stimulates chloride secretion by at least three mechanisms: (1) increasing chloride conductance across the luminal cell membrane, (2) enhancing the co-transport pathway for transmembrane movements of Na+, K+ and Cl- and (3) activating Na-K-ATPase.
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PMID:Mechanism and control of hyperosmotic NaCl-rich secretion by the rectal gland of Squalus acanthias. 614 Feb 95

Short-lasting hypothermia during thiobutabarbital general anaesthesia causes no decrease of the absolute ATP level in the blood and liver of rats. The adenylate energy charge in the tissues is relatively high - 0.86 in the liver and 0.85 in the muscles, which might be an evidence of a significant "energy sparing" during moderate hypothermia (26 +/- 1 degree C). Somatostatin in a dose of 20 micrograms/kg of body weight given to the rats during hypothermia decreased the ATP level, the ATP/ADP ratio and the adenylate energy charge in the studied tissues, especially in the liver, evidencing increased intensity of catabolic processes caused by the inhibitory action of somatostatin on the release of insulin and glucagon, among other hormones, and on the change of the insulin/glucagon ratio.
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PMID:Somatostatin effect on the level of adenyl nucleotides in the blood and tissues of rats during short-lasting hypothermia. 614 95

Electrical field stimulation of the isolated pig bladder neck preparation initiated rapid non-adrenergic, non-cholinergic nerve-mediated relaxations. A wide range of substances were examined as possible candidates for the neurotransmitter involved. Of these, only 5-hydroxytryptamine, vasoactive intestinal polypeptide, adenosine and adenosine 5'-triphosphate produced relaxations. Noradrenaline, acetylcholine, substance P, bradykinin and angiotensin II caused contraction, while neurotensin, somatostatin, bombesin and gamma-amino butyric acid were without effect. The nerve response was not blocked by methysergide, ketanserin, chymotrypsin, apamin or 8-phenyltheophylline, although methysergide antagonised the responses to 5-hydroxytryptamine, chymotrypsin blocked the responses to VIP, and 8-phenyltheophylline antagonised the responses to adenosine and ATP.
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PMID:A novel non-adrenergic, non-cholinergic nerve-mediated relaxation of the pig bladder neck: an examination of possible neurotransmitter candidates. 614 1


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