Somatostatin-14 Like Immunoreactive forms in the Rat: Characterization, Distribution and Biosynthesis

Author(s):  
Yogesh C. Patel ◽  
Hans H. Zingg ◽  
C. B. Srikant
Keyword(s):  
Endocrinology ◽  
1991 ◽  
Vol 129 (4) ◽  
pp. 2263-2265 ◽  
Author(s):  
Robert B. Mackin ◽  
Bryan D. Noe ◽  
Joachim Spiess

Biopolymers ◽  
2014 ◽  
Vol 101 (10) ◽  
pp. 1019-1028 ◽  
Author(s):  
Belén Hernández ◽  
Yves-Marie Coïc ◽  
Bruno Baron ◽  
Sergei G. Kruglik ◽  
Fernando Pflüger ◽  
...  

1992 ◽  
Vol 263 (1) ◽  
pp. R84-R88
Author(s):  
A. Bado ◽  
L. Moizo ◽  
J. P. Laigneau ◽  
M. Gauthier ◽  
M. Dubrasquet ◽  
...  

Intravenous bombesin produced a dose-related stimulation of luminal gastric somatostatin output and a concomitant dose-dependent inhibition of food intake in the gastric fistula cat. Maximal food intake inhibition was observed at 1,280 pmol.kg-1.h-1 and corresponded to 65 +/- 7% (P less than 0.01). These effects of bombesin were dose dependently abolished by the specific bombesin-receptor antagonist, [Leu13-psi(CH2NH)-Leu14]bombesin. Furthermore, intragastric administration of somatostatin-14, at doses corresponding to those found in the gastric lumen in response to intravenously administered bombesin, significantly inhibited the first 30 min of food intake. This administration had however no effect on total (daily) food intake. We therefore suggest that luminal gastric somatostatin could at least account for bombesin-induced short-term satiety.


1991 ◽  
Vol 261 (4) ◽  
pp. G693-G700 ◽  
Author(s):  
J. W. Wiley ◽  
Y. X. Lu ◽  
C. Owyang

The objective of this study was to determine whether L-glutamate (L-Glu) may serve as a neurotransmitter candidate in the guinea pig myenteric plexus. We observed that [3H]Glu and gamma-[3H]aminobutyric acid were synthesized from [3H]glutamine and released from neurons of the myenteric plexus during K+ and 1,1-dimethyl-4-phenylpiperazinium-evoked depolarization in a concentration-dependent manner. Muscle tension studies performed on ileal longitudinal muscle-myenteric plexus (LM-MP) preparations revealed that L-Glu [mean effective dose (ED50) 2.5 x 10(-5) M] produced concentration-dependent contractions, which were unaffected by hexamethonium but abolished by tetrodotoxin, atropine, and magnesium, suggesting that L-Glu acts via N-methyl-D-aspartate (NMDA)-type receptors that stimulate a cholinergic neural pathway unaffected by ganglionic blockade. In addition, L-Glu (ED50 4 x 10(-5) M) and NMDA (ED50 2 x 10(-4) M) stimulated concentration-dependent release of [3H]acetylcholine (ACh) from LM-MP sections, which was inhibited by tetrodotoxin, magnesium, and the NMDA receptor antagonist D-2-amino-5-phosphonovaleric acid (AP-5). L-Glu-mediated release of [3H]ACh was enhanced by theophylline (10-6 M) and 3-isobutyl-1-methylxanthine (1 mM) and was significantly reduced by the adenylate cyclase inhibitor, 2',5'-dideoxyadenosine (10(-4) M) and somatostatin-14 (10(-6) M), which inhibits adenosine 3',5'-cyclic monophosphate (cAMP)-dependent cholinergic transmission in the myenteric plexus. These studies suggest that L-Glu may serve as an excitatory neurotransmitter in the myenteric plexus via its action on NMDA-type receptors, which are coupled to cAMP-dependent release of ACh.


1993 ◽  
Vol 264 (5) ◽  
pp. G902-G909 ◽  
Author(s):  
G. R. Greenberg

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)


Nature ◽  
1981 ◽  
Vol 291 (5810) ◽  
pp. 76-77 ◽  
Author(s):  
Lawrence Mandarino ◽  
Debra Stenner ◽  
Wayne Blanchard ◽  
Steven Nissen ◽  
John Gerich ◽  
...  

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