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)

7 healthy subjects received an oral fat load containing 100 g neutral fat on two test days. The test meal was followed by an infusion of somatostatin (500 micrograms/h) over three hours. On the first test day 150,000 E of an active fungal lipase (extracted from Rhizopus arrhizus) were given with the fat meal. On the second day placebo capsules were administered instead of lipase. No postprandial increase of serum triglyceride levels could be found in both examinations. These results suggest, that the influence of somatostatin on triglyceride absorption cannot be due to the inhibition of pancreatic lipase secretion.
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PMID:[Further examinations of the influence of somatostatin on triglyceride absorption (author's transl)]. 610 84

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

Intravenous fluid requirements for patients with permanent end-jejunostomy syndrome often exceeds 3 L/d, making rehabilitation difficult. The effect of the somatostatin analogue, octreotide (100 micrograms TID, subcutaneously) in reducing requirements was measured in 10 patients established on home parenteral nutrition. After 10 days of treatment, 72-hour balance measurements demonstrated significant reductions in stomal fluid and electrolyte losses from (mean +/- SE) 8.1 +/- 1.8 to 4.8 +/- 0.7 L/d (p < .03), sodium from 510 +/- 71 to 340 +/- 41 mEq/d (p < .03), chloride from 533 +/- 70 to 315 +/- 32 mEq/d (p < .002), and potassium from 101 +/- 41 to 79 +/- 34 mEq/d (p < .02), permitting an average reduction in intravenous fluid requirements of 1.3 L/d (p < .0003), 118 mEq Na+/d (p < .03), 41 mEq K+/d (p < .02), and 178 mEq Cl-/d (p < .01). This meant that daytime intravenous infusions could be stopped in all patients. Fecal nitrogen losses were decreased (p < .05), but overall there was no significant change in fat and caloric absorption. In addition, hormonal stimulated gastric acid and pancreatic lipase secretions were significantly reduced (p < .05). The effect was most marked in those patients with massive stomal losses and uncontrollable thirst. Continuation of treatment for more than 1 year in 8 of the patients suggested preservation of potency and good tolerance, with the possible exception of accelerated gallstone formation and subacute intestinal obstruction. In conclusion, octreotide has the potential to improve the quality of life of those end-jejunostomy syndrome patients with massive stomal losses, resistant to conventional medical treatment.
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PMID:Octreotide as an adjunct to home parenteral nutrition in the management of permanent end-jejunostomy syndrome. 816 99

Obesity is a major public health concern and environmental factors are involved in its development. The hypothalamus is a primary site for the integration of signals for the regulation of energy homeostasis. Dysregulation of these pathways can lead to weight loss or gain. Some drugs in development can have favourable effects on body weight, acting on some of these pathways and leading to responses resulting in weight loss. Strategies for the management of weight reduction include exercise, diet, behavioural therapy, drug therapy and surgery. Investigational antiobesity medications can modulate energy homeostasis by stimulating catabolic or inhibiting anabolic pathways. Investigational drugs stimulating catabolic pathways consist of leptin, agonists of melanocortin receptor-4, 5-HT and dopamine; bupropion, growth hormone fragments, cholecystokinin subtype 1 receptor agonist, peptide YY3-36, oxyntomodulin, ciliary neurotrophic factor analogue, beta3-adrenergic receptor agonists, adiponectin derivatives and glucagon-like peptide-1. On the other hand, investigational drugs inhibiting anabolic pathways consist of the ghrelin receptor, neuropeptide Y receptor and melanin-concentrating hormone-1 antagonists; somatostatin analogues, peroxisome proliferator-activated receptor-gamma and -beta/delta antagonists, gastric emptying retardation agents, pancreatic lipase inhibitors, topiramate and cannabinoid-1 receptor antagonists. These differing approaches are reviewed and commented on in this article.
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PMID:Investigational therapies in the treatment of obesity. 1685 93

Aristaless-related homeobox gene (ARX) mutation leads to several neurological disorders including X-linked lissencephaly with abnormal genitalia (XLAG), West syndrome and Partington syndrome, with XLAG being the most severe form. Although some of the brain pathologies of XLAG have already been described, the crucial extra-brain symptoms are severe growth retardation, transient hyperglycemia and intractable diarrhea. Since ARX expresses in the islets of Langerhans during the embryonic stage, these visceral phenotypes may be related to a loss of ARX function, which develops endocrine cells in the pancreas. We investigated the abnormal pancreatic development of XLAG patients with ARX-null mutation. We performed immunohistochemistry of XLAG pancreases, using the antibodies against glucagon, insulin, somatostatin, pancreatic polypeptide, ghrelin, Brn4, Nkx2.2, Mash1, amylase and pancreatic lipase. As the results, the glucagon- and pancreatic polypeptide-producing cells were found to be completely deficient in the islets of Langerhans. We also discovered marked interstitial fibrosis, small exocrine cells with loss of amylase-producing cells and an enlargement of the central lumen of the glandular acini. These pathological findings indicate that ARX contributes not only to endocrine development, but also to exocrine development of the human pancreas, and its deficiency may lead to the severe phenotypes of XLAG patients.
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PMID:Partial loss of pancreas endocrine and exocrine cells of human ARX-null mutation: consideration of pancreas differentiation. 2053 4