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)

In 4 dogs with chronic duodenal and gastric fistulae, exocrine pancreatic function was assessed by cannulating the pancreatic duct and collecting the duodenal contents. Both methods were applied in each animal. Pancreatic secretion was stimulated by infusion of 2 CHR units of pancreozymin and secretin or by administration of a liquid test meal, injected into the stomach through the gastric fistula. During both experiments 3.5 microgram/kg somatostatin was given as bolus injection followed by an infusion of 3.5 microgram/kg/h. Somatostatin caused a significant reduction in protein and amylase output and in the bicarbonate concentration during stimulation with pancreozymin-secretin. Volume and bicarbonate slightly decreased but not to a significant extent. Duodenal volume and the duodenal activities of trypsin and amylase were significantly reduced during test meal stimulation and somatostatin infusion. Somatostatin is a potent inhibitor of exocrine pancreatic function mainly influencing enzyme secretion.
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PMID:Effect of somatostatin on exocrine pancreatic secretion stimulated by pancreozymin-secretin or by a test meal in the dog. 64 May 82

A variety of histochemical findings have contributed to a more differentiated architectonical description of the bed nucleus of the stria terminalis (BNST) in the mammalian brain. However, in the human brain investigations of the chemoarchitecture of this nucleus have been rare. Therefore we chose this region in six human autopsy brains in order to map the distribution patterns of 13 immunohistochemical markers for neurotensin (NT), neuropeptide Y (NPY), somatostatin (SOM), enkephalins (ENK), vasoactive intestinal polypeptide (VIP), substance P (SP), neurophysins (NPH), glial fibrillary acid protein, 3-fucosyl-N-acetyl-lactosamine epitope, myelin basic protein (MBP), calbindin (CAB), synaptophysin (SYN) and chromogranin-A (CHR-A). Three chemoarchitectonically distinct areas could be defined. The lateral subdivision of the BNST contained high amounts of NPY and SP-fibre immunoreactivity and was further characterized by the occurrence of neurons labelled for NPY. The central subdivision of the BNST appeared as a histochemically clearly circumscribed compartment with massive fibre immunoreactivity for SOM, ENK, VIP, SYN, CHR-A, CAB as well as SOM, ENK, NT and CAB positive cells but lacked cytosolic or fibre-like immunolabel for NPY and SP. This structure was also ensheathed by myelinated fibres identified by means of MBP immunohistochemistry. The medial subdivision of the BNST showed moderate to high SP and NPY fibre immunoreactivity but lacked immunolabelled neurons and was only scarcely supplied with varicose or punctiform ENK immunoproduct. In the most posterior levels of our sections a cell group labelled for NPH was located lateral to the fornix columns. The lateral subdivision of the BNST (with NPY, SYN) and mainly the central BNST (with SOM, ENK, VIP, SYN and CHR-A) contributed to ventrolateral extensions of dense patchy fibre immunoreactivity throughout the basal forebrain region.
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PMID:Differential distribution of immunohistochemical markers in the bed nucleus of the stria terminalis in the human brain. 171 18

A somatostatin analogue (SMS-201-995, hereinafter "octreotide") was s.c. administered to 5 healthy subjects under consecutive dripping of CCK-PZ (cholecystokinin-pancreozymin) and secretin (0.01 CHR U/kg/minutes), after inserting a Dreiling double tube into Treitz's ligament. Bile acid concentration, and bicarbonate and lipase excretions in duodenal juice were determined every 10 minutes up to 120 minutes and compared with controls. Moreover, octreotide (100 micrograms) was s.c. administered to 5 healthy subjects 30 minutes before meals for 7 days. Fecal fat and bile acid excretions before and after administration were determined. Bile acid concentration, and bicarbonate and lipase excretions in the octreotide group decreased to 1/3-1/4 that of controls. Bile acid concentration became 0 mM for 60 minutes. Fecal fat excretion increased; obvious steatorrhea occurred in 2 cases. Fecal bile acid excretion decreased to about 1/4. These results suggest that decreases in bile acid secretion should be considered, as well as pancreatic lipase and bicarbonate secretions, when fatty stool occurs after octreotide administration.
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PMID:Octreotide decreases biliary and pancreatic exocrine function, and induces steatorrhea in healthy subjects. 782 73