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Mark A Sheridan - One of the best experts on this subject based on the ideXlab platform.

  • Effects of insulin, glucagon, and Somatostatin on the release of Somatostatin-25 and Somatostatin-14 from rainbow trout, Oncorhynchus mykiss, pancreatic islets in vitro.
    General and comparative endocrinology, 1995
    Co-Authors: C. D. Eilertson, Jeffrey D. Kittilson, Mark A Sheridan
    Abstract:

    Somatostatins are a diverse family of peptides known to modulate insulin and glucagon secretion as well as to stimulate glycogenolysis and lipolysis in salmonid fish. In this study, Brockmann bodies (bisected to yield hemi-islets) isolated from rainbow trout, Oncorhynchus mykiss, were used to study the effects of insulin, glucagon, and Somatostatin at various concentrations of glucose (1, 5, and 10 mM) on pancreatic Somatostatin release. The release of Somatostatin-25, the most predominate form of Somatostatin in salmonid pancreas, was stimulated by insulin in the presence of 1 and 5 mM glucose but not in the presence of 10 mM glucose, whereas glucagon stimulated Somatostatin-25 release only in the presence of high (10 mM) glucose. Somatostatin-25 release also was stimulated by Somatostatin-14. The secretion of Somatostatin-14 was suppressed by insulin in the presence of 5 and 10 mM glucose and was stimulated by glucagon in the presence of high (10 mM) glucose. These results indicate that insulin, glucagon, and Somatostatin-14 are regulators of Somatostatin-14 and Somatostatin-25 pancreatic release in rainbow trout and that these effects are modulated by glucose.

  • Effects of Somatostatin-25 on lipid mobilization from rainbow trout, Oncorhynchus mykiss, liver and adipose tissue incubated in vitro. Comparison with Somatostatin-14
    Journal of Comparative Physiology B-biochemical Systemic and Environmental Physiology, 1994
    Co-Authors: C. D. Eilertson, Mark A Sheridan
    Abstract:

    The physiological effects of the pancreatic peptides Somatostatin-14 and Somatostatin-25 on lipid metabolism in rainbow trout were evaluated by in vitro culture of liver and adipose tissue. The culture medium was subsequently analyzed for glycerol and fatty acid content and triacylglycerol lipase activity was measured within the tissues. Both Somatostatin-14 and Somatostatin-25 stimulated hepatic fatty acid and glycerol release within 3 h after treatment. Liver triacylglycerol lipase activity was elevated following treatment with Somatostatin-14 (76% above control) or Somatostatin-25 (94% above control). Somatostatin-14 and Somatostatin-25 also significantly stimulated the release of fatty acid and glycerol from adipose tissue. Triacylglycerol lipase activity in adipose tissue also was enhanced by both Somatostatins. These results indicate that Somatostatin-14 and Somatostatin-25 directly stimulate the mobilization of triacylglycerol from liver and adipose tissue, suggesting that these peptides are important systemic modulators of lipid metabolism in fish.

  • Differential Effects of Somatostatin-14 and Somatostatin-25 on Carbohydrate and Lipid Metabolism in Rainbow Trout Oncorhynchus mykiss
    General and comparative endocrinology, 1993
    Co-Authors: Carmen D. Eilertson, Mark A Sheridan
    Abstract:

    Abstract Previous studies have indicated that teleost fish appear to have two Somatostatin genes. In salmonid fish, it is purported that gene I encodes for Somatostatin-14 (SS-14), while gene II encodes for Somatostatin-25 (sSS-25). In the present study, the physiological effects of SS-14 and sSS-25 on carbohydrate and lipid metabolism in rainbow trout, Oncorhynchus mykiss , were evaluated by in vivo administration of hormone and measuring resulting levels of specific metabolites and hormones present within tissues and plasma. Somatostatin-14 administration caused hyperglycemia without affecting liver glycogen content and increased plasma fatty acid (FA) levels in association with enhanced activity of the lipid mobilizing enzyme, triacylglycerol lipage (TG lipase). Somatostatin-14 injection also resulted in reduced hepatic glucose-6-phosphate dehydrogenase activity, which may indicate a decrease in glucose channeling through the pentose phosphate shunt. In addition, SS-14 reduced plasma glucagon concentration, while having no effect on plasma insulin levels. Salmon SS-25 elevated plasma glucose levels in association with reduced glycogen content and resulted in increased plasma FA levels accompanied by increased hepatic TG lipase activity. Salmon SS-25 injection also resulted in a reduction in plasma glucagon and insulin levels. These results indicate that SS-14 and sSS-25 are important regulators of carbohydrate and lipid metabolism in rainbow trout and that modulation of metabolic activity by these peptides may be accomplished, in part, by alterations in insulin and glucagon levels circulating in the plasma.

Gordon R. Greenberg - One of the best experts on this subject based on the ideXlab platform.

  • cholecystokinin type a receptors mediate intestinal fat induced inhibition of acid secretion through Somatostatin 14 in dogs
    Endocrinology, 1994
    Co-Authors: Leslie C. Fung, Sherry Pokoldaniel, Gordon R. Greenberg
    Abstract:

    This study was designed to examine whether one or both principle molecular forms of Somatostatin (SLI), Somatostatin-28 (S-28) and Somatostatin-14 (S-14), mediate inhibition of stimulated gastric acid by intestinal fat and to determine whether the mode of action includes activation of type A cholecystokinin (CCK) receptors in conscious dogs. SLI molecular forms were separated by gel filtration chromatography after extraction of acidified plasma on octadecyl silyl cartridges and quantified by RIA. Basal plasma levels of S-28 and S-14 were 4.1 +/- 0.6 and 3.6 +/- 0.3 fmol/ml, respectively. Intraduodenal perfusion with a 10% fat emulsion increased plasma S-28 by 6.3 +/- 1.2 fmol/ml (P < 0.01) and S-14 by 17.8 +/- 2.6 fmol/ml (P < 0.001), and suppressed by 76 +/- 3% (P < 0.001) gastrin (150 pmol/kg.h)-stimulated gastric acid. Blockade of type A CCK receptors with MK-329 (75 micrograms/kg, i.v.) abolished S-28 and S-14 responses (both P < 0.001) and completely reversed the inhibitory effect of gastric acid pro...

  • Differential neural regulation of circulating Somatostatin-14 and Somatostatin-28 in conscious dogs.
    American Journal of Physiology-Gastrointestinal and Liver Physiology, 1993
    Co-Authors: Gordon R. Greenberg
    Abstract:

    Somatostatin-like immunoreactivity (SLI) released into the circulation after nutrients or secretagogues is heterogeneous. To determine whether similar neural pathways regulate secretion of SLI molecular forms, circulating Somatostatin-28 (S-28) and Somatostatin-14 (S-14) responses to ingestion of a solid meal, intraduodenal perfusion of a liquid defined formula meal, and intravenous infusion of cholecystokinin octapeptide (CCK-OP, 250 pmol.kg-1.h-1) were measured in four conscious dogs with and without cryogenic blockade of the cervical vagus nerves. SLI was separated by gel-filtration chromatography of extracted, acidified plasma and quantified by radioimmunoassay. Basal plasma concentrations of S-28 were 4.1 +/- 0.6 fmol/ml and of S-14 were 3.8 +/- 0.4 fmol/ml. Ingestion of the solid meal increased plasma SLI threefold, and elevations of S-28 and S-14 were equivalent. After the intraduodenal liquid meal or infusion of CCK-OP, plasma SLI rose twofold, but increments of S-28 exceeded S-14, comprising approximately 70% of SLI released. Vagal blockade by cooling reversibly inhibited both the S-28 and S-14 responses to the solid meal, intraduodenal liquid meal, and CCK-OP. In contrast, atropine (50 micrograms/kg iv), given after solid food, intraduodenal nutrients, and CCK-OP, suppressed S-28 but further increased S-14 responses. Atropine did not, however, alter the suppression of S-14 and S-28 by vagal cooling.(ABSTRACT TRUNCATED AT 250 WORDS)

  • Regulation of Somatostatin-14 and -28 secretion by gastric acid in dogs: Differential role of cholecystokinin
    Gastroenterology, 1993
    Co-Authors: Gordon R. Greenberg, Leslie C. Fung, Sherry Pokol-daniel
    Abstract:

    Abstract Background: ProSomatostatin-derived peptides include two principle bioactive molecular forms, Somatostatin 28 (S-28) and Somatostatin 14 (S-14). This study examined whether there is a functional relationship between gastric acid secretion and the release of S-28 and S-14 into the circulation. Methods: In conscious dogs with gastric and duodenal cannulas, S-28 and S-14 responses, measured after extraction of acidified plasma and separation by gel chromatography, were evaluated by administration of nutrients and acid-inducing secretagogues without and with omeprazole. Results: Ingestion of a solid meal caused equivalent plasma elevations of S-28 and S-14, whereas infusions of histamine and gastrin selectively increased plasma S-14. Omeprazole decreased meal-stimulated S-28 (−67% ± 8%; P P P P Conclusions: In the fed state, gastric acid causes direct release of S-14 from the stomach, but the acid-dependent component of S-28 secretion requires cholecystokinin as a cofactor. Negative feedback regulation between Somatostatin and gastric acid secretory responses to nutrients may include S-28 modulated, in part, by cholecystokinin.

Hyman B Niznik - One of the best experts on this subject based on the ideXlab platform.

  • a human Somatostatin receptor sstr3 located on chromosome 22 displays preferential affinity for Somatostatin 14 like peptides
    FEBS Letters, 1993
    Co-Authors: Jacquie D Corness, Yogesh C. Patel, Lidia Demchyshyn, Philip Seeman, Hubert H M Van Tol, Coimbatore B Srikant, Gillian Kent, Hyman B Niznik
    Abstract:

    We report here on the cloning of a human intronless gene encoding a member of the G-protein linked Somatostatin (SST) receptor subfamily, termed SSTR3. Based on the deduced amino acid sequence, this gene encodes a 418 amino acid protein displaying sequence similarity, particularly within putative transmembrane domains, with the recently cloned human SSTR1 (62%), SSTR2 (64%) and SSTR4 (58%) receptors. Membranes prepared from COS-7 cells transiently expressing the human SSTR3 gene bound [125I]Leu8,d-Trp22,-Tyr22 SST-28 in a saturable manner with high affinity (~200 pM) and with rank order of potency (d-Trp8 SST-14 > SST-14 > SMS-201-995 > SST-28) indicative of a Somatostatin-14 selective receptor. The pharmacological profile of the expressed human SSTR3 receptor is similar but not identical to that reported for the rat homolog [(1992) J. Biol. Chem. 267,20422] where the peptide selectivity is SST-28 ≧ SST-14 XXX SMS-201-995. Northern blot analysis reveals the presence of an SSTR3 mRNA species of ~5 kb in various regions of the monkey brain, including the frontal cortex, cerebellum, medulla, amygdala, with little or no SSTR3 mRNA detectable in brain regions such as the striatum, hippocampus, and olfactory tubercle. The SSTR3 receptor gene maps to human chromosome 22. The existence of at least four distinct human genes encoding Somatostatin-14 selective receptors with diverse pharmacological specificities may help to account for some of the multiple biological actions of Somatostatin under normal and pathological conditions.

  • A human Somatostatin receptor (SSTR3), located on chromosome 22, displays preferential affinity for Somatostatin‐14 like peptides
    FEBS letters, 1993
    Co-Authors: Jacquie D Corness, Yogesh C. Patel, Lidia Demchyshyn, Philip Seeman, Hubert H M Van Tol, Coimbatore B Srikant, Gillian Kent, Hyman B Niznik
    Abstract:

    We report here on the cloning of a human intronless gene encoding a member of the G-protein linked Somatostatin (SST) receptor subfamily, termed SSTR3. Based on the deduced amino acid sequence, this gene encodes a 418 amino acid protein displaying sequence similarity, particularly within putative transmembrane domains, with the recently cloned human SSTR1 (62%), SSTR2 (64%) and SSTR4 (58%) receptors. Membranes prepared from COS-7 cells transiently expressing the human SSTR3 gene bound [125I]Leu8,d-Trp22,-Tyr22 SST-28 in a saturable manner with high affinity (~200 pM) and with rank order of potency (d-Trp8 SST-14 > SST-14 > SMS-201-995 > SST-28) indicative of a Somatostatin-14 selective receptor. The pharmacological profile of the expressed human SSTR3 receptor is similar but not identical to that reported for the rat homolog [(1992) J. Biol. Chem. 267,20422] where the peptide selectivity is SST-28 ≧ SST-14 XXX SMS-201-995. Northern blot analysis reveals the presence of an SSTR3 mRNA species of ~5 kb in various regions of the monkey brain, including the frontal cortex, cerebellum, medulla, amygdala, with little or no SSTR3 mRNA detectable in brain regions such as the striatum, hippocampus, and olfactory tubercle. The SSTR3 receptor gene maps to human chromosome 22. The existence of at least four distinct human genes encoding Somatostatin-14 selective receptors with diverse pharmacological specificities may help to account for some of the multiple biological actions of Somatostatin under normal and pathological conditions.

Mileva V. Mićić - One of the best experts on this subject based on the ideXlab platform.

  • Changes in thymus size, cellularity and relation between thymocyte subpopulations in young adult rats induced by Somatostatin-14.
    Neuropeptides, 2007
    Co-Authors: Danica M. Petrović-Đergović, Ana Rakin, Ljiljana A. Dimitrijevic, Jasmina S. Ristovski, Natasa Kustrimovic, Mileva V. Mićić
    Abstract:

    Abstract The role of Somatostatin on inhibition of both normal and tumor cell cycle, secretion of endocrine and exocrine cells, as well as induction apoptosis is well documented. However, its effect on T cell development and thymic structure is not fully clarified. In order to investigate the influence of Somatostatin in vivo on the thymus structure and T cell development, the young adult Albino Oxford male rats were intracerebroventriculary treated with Somatostatin-14. We examined the thymus compartments and its cellularity, through assessment of morphometric parameters by stereological method, and the relation between thymocytes subpopulations, over expression of CD4, CD8 and T-cell receptor (TCR) αβ by flow cytometry. Additionally, we also determined the body and thymus weight of the rats, during the first three months of life, to define the time of SRIH-14 application. A decrease of relative thymus weight from the fourth weeks of postnatal life, and an unchanged relative thymus weight obtained in treated group indicates that SRIH-14 in young adult rats inhibits growth of whole organism, not only thymus. The changes in the absolute number and numerical density of cortical thymocytes indicate that SRIH-14 alters the true lymphoid tissue. SRIH-14 changes relation between thymocyte subsets, increase number of CD4 − CD8 − TCRαβ − and CD4 − CD8 + TCRαβ hi thymocyte subsets as well as the CD4 − CD8 − TCRαβ low/hi thymocytes, while decrease number of CD4 + CD8 + TCRαβ −/low/hi thymocyte subsets. These results indicate that Somatostatin-14 is not involved in the control of the physiologic involution of the thymus, although induces thymic weight loss through the reduction of true lymphoid tissue. In addition, changes in frequency of thymocyte subpopulations, especially immature cells, indicate that SRIH-14 modulates thymocytes development and maturation.

  • Somatostatin-14 alters the thymus size and relation among the thymocyte subpopulations in peripubertal rats.
    Neuropeptides, 2004
    Co-Authors: D.m. Petrovic-Đergovic, I.p. Živković, Ana Rakin, D.j. Kosec, Lj.a. Dimitrijević, Vesna Starcevic, Walter B. Severs, Mileva V. Mićić
    Abstract:

    Abstract It is well known that Somatostatin exerts a wide range of effects in the body, and acts as an autocrine or paracrine factor in the thymus. However, it has not been investigated yet whether Somatostatin alters the thymus size and relation among the thymocyte subpopulations in the peripubertal rats. For this purpose, the peripubertal AO male rats were cannulated intracerebroventriculary and treated with repeated, low doses of Somatostatin-14 (experimental group) or saline (control group). Twenty-four hours after the last treatment, we removed and prepared the thymuses for determination of thymocyte subpopulations by flow cytometry. After five days, animals were sacrificed and their thymuses taken for morphometrical analysis by stereological methods. We noticed that Somatostatin-14 decreased volumes of thymus cortex and medulla, total number of thymocytes, number of thymocytes in the cortex and medulla and numerical density of thymocytes in deeper cortex. As a consequence of these changes, thymus size was also diminished. The phenotypic analysis of thymocyte subpopulations showed that Somatostatin-14 decreased the percentage of CD4 + CD8 + cells with low level of TCRαβ expression, positively selected CD4 + CD8 + TCRαβ high cells and the most mature CD4 − CD8 + TCRαβ high cells, while the percentage of CD4 + CD8 − TCRαβ high thymocytes was slightly increased. Somatostatin-14 increased the relative proportion of the least mature CD4 − CD8 − TCRαβ −/low , CD4 + CD8 + TCRαβ − cells and both of TCRαβ −/low single positive subpopulations. These results show that centrally applied Somatostatin-14, induces hypotrophy of the thymus in peripubertal rats by changing the volumes and cellularities of the thymic compartments. Additionally, increased number of the least mature thymocytes and a deficiency of double positive cells indicate the involvement of Somatostatin in the modulation of T cells maturation.

C. D. Eilertson - One of the best experts on this subject based on the ideXlab platform.