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

We studied the release of immunoreactive somatostatin, VIP, and galanin during net aboral propulsive complexes (NAP) in isolated, perfused, 80-cm segments of porcine ileum. Net aboral propulsive complexes were induced by controlled infusion of liquid (perfusion medium, 3.5 ml/min) into the proximal opening of the ileum segment. In response to liquid infusion, the ileum segments generated propulsive complexes rapidly propagating along the entire segment in the aboral direction, resulting in emptying of the luminal contents. The NAPs occurred with an average interval of 7 minutes. The concentrations of galanin, somatostatin, and VIP in the venous effluent, which in control experiments without luminal infusion did not change, increased significantly (by 63.6 +/- 23.7%, 43.8 +/- 31.8%, and 38.8 +/- 14.6%, respectively) during NAPs and emptying. Atropine (10(-6) mol/l) and hexamethonium (10(-5) mol/l) abolished both NAP generation and peptide responses. It is concluded that the enteric neuropeptides, somatostatin, VIP, and galanin, all of which have pronounced intestinal motor effects, may participate in the generation of net aboral propulsive complexes in the ileum of the pig, possibly mainly in descending relaxation.
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PMID:Release of immunoreactive somatostatin, vasoactive intestinal polypeptide (VIP), and galanin during propulsive complexes in isolated pig ileum. 768 99

The role of somatostatin-14 in duodenal mucosal HCO3- secretion was investigated in anesthetized, indomethacin-treated guinea pigs. Net HCO3- output from the isolated, perfused (24 mM NaHCO3 + 130 mM NaCl) proximal duodenum was measured during intravenous infusion (alone or in combination) of somatostatin-14, carbachol, vasoactive intestinal peptide (VIP), and prostaglandin E2 (PGE2). In homogenates of duodenal enterocytes, the effect of these agents on adenylate cyclase activity was studied. Basal duodenal HCO3- secretion (3.5 +/- 0.2 mumol/cm/10 min) was reduced dose dependently by somatostatin-14 (10(-11) mol/kg, 10(-9) mol/kg, and 10(-7) mol/kg). Carbachol, VIP, and PGE2 (all 10(-8) mol/kg) increased basal duodenal HCO3- secretion two- to threefold. Somatostatin-14 (10(-7) mol/kg) abolished the stimulatory effect of carbachol and VIP, but not that of PGE2. Basal adenylate cyclase activity in isolated duodenal enterocytes (9.4 +/- 1.0 pmol cAMP/mg protein/min) was unaltered by somatostatin (10(-6) mol/liter) or carbachol (10(-3) mol/liter). VIP (10(-8) mol/liter) and PGE2 (10(-7) mol/liter) increased adenylate cyclase activity two- to threefold, and these effects were unchanged by somatostatin-14 (10(-6) mol/liter). In conclusion, somatostatin-14 inhibits basal and carbachol- and VIP-stimulated duodenal HCO3- secretion, and its mechanism of action is not via inhibition of adenylate cyclase activity in duodenal enterocytes.
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PMID:Effect of somatostatin-14 on duodenal mucosal bicarbonate secretion in guinea pigs. 789 65

The present study was undertaken to determine whether an acute physiologic rise in plasma cortisol during selective insulin deficiency would have significant effects on glycerol and beta-hydroxybutyrate metabolism in conscious overnight-fasted dogs. Each experiment consisted of a two hour dye equilibration period, a 40 minute basal period, and a 3 hour experimental period. A continuous infusion of indocyanine green dye for blood flow estimation was initiated at the start of the equilibration period and continued throughout the experiment. In both of two protocols selective insulin deficiency was created during the experimental period by infusing somatostatin peripherally (0.8 microgram/kg-min) with basal replacement of glucagon intraportally (0.65 ng/kg-min). In the test protocol (CORTISOL, n = 5), 3.0 micrograms/kg-min of hydrocortisone was infused during the experimental period. In the control protocol (SALINE, n = 5), saline was infused. Net hepatic balances were determined using the (A-V) difference technique. During selective insulin deficiency alone (SALINE), the arterial blood glycerol level increased from 81 +/- 19 to 140 +/- 11 microM (p < 0.01) and net hepatic glycerol uptake (NHGlyU) tended to increase from 2.3 +/- 0.3 to 3.3 +/- 0.6 mumol/kg-min (0.05 < 0.1). The arterial plasma free fatty acid (FFA) level remained unchanged at 1041 +/- 35 microM. The arterial beta-hydroxybutyrate (BHOB) level increased slightly from 21 +/- 4 to 29 +/- 5 microM while net hepatic beta-hydroxybutyrate production (NHBP) remained unchanged (1.0 +/- 0.2 mumol/kg-min). During acute hypercortisolemia with selective insulin deficiency (CORTISOL), similar changes occurred in the arterial blood glycerol level and net hepatic glycerol uptake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of acute hypercortisolemia on beta-hydroxybutyrate and glycerol metabolism during insulin deficiency. 790 56

In order to investigate the properties of somatostatin-14 we studied an experimental model of simple mechanical and closed loop occlusion. Forty-eight New Zealand rabbits were assigned randomly to three groups of 16: group C (controls) was operated and treated with saline solution (4 cc/Kg/h); group A was operated and initially treated with saline solution and an equal dose of somatostatin-14 (3.5 micrograms/Kg/h; and group B was operated and treated in the same manner as group A, but later, 8 hours after the laparotomy. The animals were sacrificed 24 hours later; intestinal secretion was quantified, blood and intestinal fluid chemistries were performed and specimens of the intestine were prepared for histological examination. Descriptive statistical analysis of the results was performed with the ANOVA, a semi-quantitative test and the covariance test. Somatostatin-14 produced an improvement in the volume of intestinal secretion in the treated groups compared with the control group. The results were statistically significant in group B treated after an 8-hour delay: closed loop (ml): 6.40 +/- 1.12, 2.50 +/- 0.94, 1.85 +/- 0.83 and simple mechanical occlusion (ml): 175 +/- 33.05, 89.50 +/- 9.27, 57.18 +/- 21.23, p < 0.01 for groups C, A and B C, A and B respectively. Net secretion of Cl and Na ions was also improved, p < 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of somatostatin-14 in simple mechanical obstruction of the small intestine]. 791 73

To investigate the temporal response of the liver to insulin and portal glucose delivery, somatostatin was infused into four groups of 42-h-fasted, conscious dogs (n = 6/group), basal insulin and glucagon were replaced intraportally, and hyperglycemia was created via a peripheral glucose infusion for 90 min (period 1). This was followed by a 240-min experimental period (period 2) in which hyperglycemia was matched to period 1 and either no changes were made (CON), a fourfold rise in insulin was created (INS), a portion of the glucose (22.4 mumol.kg-1.min-1) was infused via the portal vein (Po), or a fourfold rise in insulin was created in combination with portal glucose infusion (INSPo). Arterial insulin levels were similar in all groups during period 1 (approximately 45 pM) and were 45 +/- 9, 154 +/- 20, 43 +/- 7, and 128 +/- 14 pM during period 2 in CON, INS, Po, and INSPo, respectively. The hepatic glucose load was similar between periods and among groups (approximately 278 mumol.kg-1.min-1). Net hepatic glucose output was similar among groups during period 1 (approximately 0.1 mumol.kg-1.min-1) and did not change significantly in CON during period 2. In INS net hepatic glucose uptake (NHGU; mumol.kg-1.min-1) was -3.8 +/- 3.3 at 15 min of period 2 and did not reach a maximum (-15.9 +/- 6.6) until 90 min. In contrast, NHGU reached a maximum of -13.0 +/- 3.7 in Po after only 15 min of period 2. In INSPo, NHGU reached a maximum (-23.6 +/- 3.5) at 60 min. Liver glycogen accumulation during period 2 was 21 +/- 10, 84 +/- 17, 65 +/- 16, and 134 +/- 17 mumol/gram in CON, INS, Po, and INSPo, respectively. The increment (period 1 to period 2) in the active form of liver glycogen synthase was 0.7 +/- 0.4, 6.5 +/- 1.2, 2.8 +/- 1.0, and 8.5 +/- 1.3% in CON, INS, Po, and INSPo, respectively. Thus, in contrast to insulin, the portal signal rapidly activates NHGU. In addition, the portal signal independent of a rise in insulin, can cause glycogen accumulation in the liver.
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PMID:Comparison of the time courses of insulin and the portal signal on hepatic glucose and glycogen metabolism in the conscious dog. 855 Aug 54

The role of the liver nerves in the disposition of peripherally administered glucose was examined in seven hepatic innervated (HI) and nine hepatic denervated (HD) 42-h-fasted conscious dogs. After a 40-min basal period, there was a 4-h experimental period during which the hepatic glucose load was increased twofold via peripheral glucose infusion. Somatostatin was infused to suppress pancreatic endocrine secretion, and insulin and glucagon were infused intraportally to produce a fourfold increase in insulin and a gradual decrease (approximately 25%) in glucagon. The area under the curve of net hepatic glucose uptake (NHGU) during the glucose infusion period totaled 483 +/- 82 and 335 +/- 32 mg/kg in HD and HI, respectively (P < 0.05). The area under the curve of the hepatic fractional extraction of glucose was 27% greater in HD (P < 0.05). Net hepatic lactate output was similar in the two groups, and net hepatic glycogen synthesis was 3.8 +/- 0.8 vs. 2.7 +/- 0.5 mg.kg dog wt-1.min-1 in HD and HI, respectively (P = 0.13). The direct pathway of glycogen synthesis was responsible for 54-58% of net hepatic glycogen synthesis in both HI and HD (n = 6 for both). In summary 1) NHGU in response to peripheral glucose infusion was approximately 44% greater in HD than in HI, 2) net hepatic glycogen synthesis was enhanced by 41% in HD although the probability of this change was 0.13, and 3) the contribution of the direct pathway to glycogen synthesis was the same in HD and HI. These data are consistent with a role for the liver nerves in regulating the magnitude of NHGU in response to glucose administration. They also indicate that the absence of liver nerves may reduce glycogen turnover during glucose infusion.
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PMID:Neural and pancreatic influences on net hepatic glucose uptake and glycogen synthesis. 877 13

We investigated the mechanisms by which peripheral or portal insulin can independently alter liver glucose production. Isotopic ([3-3H]glucose) and arteriovenous difference methods were used in conscious overnight-fasted dogs. A pancreatic clamp (somatostatin plus basal insulin and basal glucagon infusions) was used to control the endocrine pancreas. After a 40-min basal period, a 180-min experimental period followed in which selective increases in peripheral (PERI group, n = 5) or portal-vein (PORT group, n = 5) insulin were induced. In control dogs (CONT group, n = 10), insulin was not increased. Glucagon levels were fixed in all studies, and basal euglycemia was maintained by peripheral glucose infusion in the two experimental groups. In the PERI group, arterial insulin rose from 36 +/- 12 to 120 +/- 12 pmol/l, while portal insulin was unaltered. In the PORT group, portal insulin rose from 108 +/- 42 to 192 +/- 42 pmol/l, while arterial insulin was unaltered. Neither arterial nor portal insulin changed from basal in the CONT group. With a selective rise in peripheral insulin, the net hepatic glucose output (NHGO; basal, 11.8 +/- 0.7 micromol x kg-1 x min-1) did not change initially (11.8 +/- 2.1 micromol x kg-1 x min-1, 30 min after the insulin increase), but eventually fell (P < 0.05 ) to 6.1 +/- 0.9 micromol x kg-1 x min-1 (last 30 min). With a selective rise in portal insulin, NHGO dropped quickly (P < 0.05) from 10.0 +/- 0.9 to 5.6 +/- 0.6 micromol x kg-1 x min-1 (30 min after the insulin increase) and eventually reached 3.1 +/- 1.1 micromol x kg-1 x min-1 (last 30 min). When insulin levels were not increased (CONT group), NHGO dropped progressively from 10.1 +/- 0.6 to 8.3 +/- 0.6 micromol x kg-1 x min-1 (last 30 min). Conclusions drawn from the net hepatic glucose balance data were confirmed by the tracer data. Net hepatic gluconeogenic substrate uptake (three carbon precursors) fell 2.0 micromol x kg-1 x min-1 in the PERI group, but rose 1.2 micromol x kg-1 x min-1 in the PORT group and 1.2 micromol x kg-1 x min-1 in the CONT group. A selective 84 pmol/l rise in arterial insulin was thus associated with a fall in NHGO of approximately 50%, which took 1 h to manifest. Conversely, a selective 84 pmol/l rise in portal insulin was associated with a 50% fall in NHGO, which occurred quickly (15 min). From the control data, it is evident that in either case approximately 30% of the fall in NHGO was due to a drift down in baseline and that 70% was due to the rise in insulin. In conclusion, an increment in portal insulin had a rapid inhibitory effect on NHGO, caused by the suppression of glycogenolysis, while an equal increment in arterial insulin produced an equally potent but slower effect that resulted from a small increase in hepatic sinusoidal insulin, from a suppression of gluconeogenic precursor uptake by the liver, and from a redirection of glycogenolytic carbon to lactate rather than glucose.
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PMID:A comparison of the effects of selective increases in peripheral or portal insulin on hepatic glucose production in the conscious dog. 886 66

The chronic and acute roles of hyperglucagonemia in sustaining the increased glucose production observed in the conscious infected dog were examined. Three groups of dogs were studied: a sham group (SHAM; n = 10), an infected group (INFXN; n = 11), and a sham group in which the chronic (42-h) increase in glucagon observed in INFXN was simulated (SimGGN; n = 5). INFXN and SimGGN were studied in the presence of hyperglucagonemia. In addition, glucagon was selectively decreased for 180 min in INFXN by use of somatostatin with basal intraportal insulin replacement and in SimGGN by discontinuing the exogenous glucagon infusion. Tracer and arteriovenous difference techniques were used to assess hepatic glucose metabolism and gluconeogenesis. Whereas the rate of glucose appearance (Ra) was increased by 30% (3.3 +/- 0.1 vs. 2.5 +/- 0.1 mg.kg-1.min-1) in INFXN vs. SHAM, Ra did not increase in SimGGN (2.4 +/- 0.2 mg.kg-1.min-1). In addition, the 30% increase in net hepatic gluconeogenic precursor uptake seen in INFXN did not occur in SimGGN despite an augmented net hepatic alanine fractional extraction (0.62 +/- 0.03 vs. 0.47 +/- 0.05, SimGGN vs. INFXN). With acute removal of hyperglucagonemia, endogenous Ra decreased in SimGGN and INFXN by 1.0 +/- 0.2 and 1.4 +/- 0.3 mg.kg-1.min-1, respectively. Net hepatic alanine fractional extraction in INFXN, leading to a greater rise in arterial blood alanine levels. In summary, chronic hyperglucagonemia alone cannot explain the increase in Ra observed during an infection. The marked hyperglucagonemia seen during infection plays an essential role in sustaining normal net hepatic fractional alanine extraction to compensate for an impairment in glucagon-stimulated hepatic amino acid transport activation.
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PMID:Hyperglucagonemia and hepatic glucose metabolism during infection in the conscious dog. 892 62

We used eight Polypay wethers (36 +/- .6 kg BW) fitted with hepatic portal, hepatic venous, mesenteric arterial and venous, and duodenal catheters in a crossover design experiment to determine the influence of somatostatin (SRIF) on splanchnic metabolism. Each crossover period consisted of 14 d, with net flux of nutrients and hormones (venoarterial differences x blood flow) measured on d 14. Before flux measurements, wethers received an i.v. dose (0 h) of either 0 (vehicle) or 50 mg x kg BW(-1) x 10 min(-1) cysteamine (CSH, SRIF-depleting agent) followed by a continuous duodenal infusion (h 10 to 22) of a starch hydrolysate-casein solution. Six sets of arterial, portal, and hepatic blood samples were obtained (h 12 to 16), after which a primed (10 microg), continuous jugular infusion of SRIF-14 (5.0 microg x kg BW(-1) x h(-1)) was initiated and sampling protocol repeated (h 18 to 22). Cysteamine administration increased (P < .01, vs control) portal and hepatic blood flow in the absence of exogenous SRIF (CSH x SRIF, P < .01). Net portal-drained viscera (PDV) release of glucose, alpha-amino N, ammonia N, beta-hydroxybutyrate, and oxygen consumption were decreased (P < or = .10) and lactate release increased (P = .005) during SRIF infusion. The CSH increased (P < .05) PDV release of beta-hydroxybutyrate and insulin and increased (P = .09, CSH alone vs control) net release of glucose in the absence of exogenous SRIF. Exogenous SRIF increased (P = .10) and CSH decreased (P = .09) net hepatic glucose output, whereas liver oxygen consumption was decreased (P = .04) with exogenous SRIF and increased (P = .01) with CSH. Net total splanchnic alpha-amino N release and oxygen consumption were decreased (P < .10) with exogenous SRIF, but CSH increased (P < .05) insulin release and oxygen consumption. These data provide initial evidence for a regulatory involvement of SRIF in visceral metabolism in ruminants.
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PMID:Effects of exogenous somatostatin and cysteamine on net nutrient flux across the portal-drained viscera and liver of sheep during intraduodenal infusion of starch hydrolysate and casein. 937 19

Concomitant portal infusion of gluconeogenic amino acids (GNGAA) and glucose significantly reduces net hepatic glucose uptake (NHGU), in comparison with NHGU during portal infusion of glucose alone. To determine whether this effect on NHGU is specific to the portal route of GNGAA delivery, somatostatin, intraportal insulin (3-fold basal) and glucagon (basal), and intraportal glucose (to increase the hepatic glucose load by approximately 50%) were infused for 240 min. GNGAA were infused peripherally into a group of dogs (PeAA), at a rate to match the hepatic GNGAA load in a group of dogs that were given the same GNGAA mixture intraportally (PoAA) at 7.6 micromol. kg-1. min-1 (9). The arterial blood glucose concentrations and hepatic glucose loads were the same in the two groups, but NHGU (-0. 9 +/- 0.2 PoAA and -2.1 +/- 0.5 mg. kg-1. min-1 in PeAA, P < 0.05) and net hepatic fractional extraction of glucose (2.6 +/- 0.7% in PoAA vs. 5.9 +/- 1.4% in PeAA, P < 0.05) differed. Neither the hepatic loads nor the net hepatic uptakes of GNGAA were significantly different in the two groups. Net hepatic glycogen synthesis was approximately 2.5-fold greater in PeAA than PoAA (P < 0.05). Intraportal, but not peripheral, amino acid infusion suppresses NHGU and net hepatic glycogen synthesis in response to intraportal glucose infusion.
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PMID:Differential effect of amino acid infusion route on net hepatic glucose uptake in the dog. 995 Jul 89


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