Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The long acting somatostatin analogue octreotide acetate has been effective in the treatment of early dumping syndrome. We hypothesized that this may be related to its effects on inhibiting gastric emptying and delaying intestinal transit. To study the effect of octreotide acetate on intestinal motility in patients we carried out a randomized, double-blinded study using a subcutaneous injection of either octreotide acetate (100 micrograms) or placebo given 20 min prior to ingestion of a high carbohydrate "dumping" meal in six patients with known severe dumping syndrome. Prior to each study a multilumen polyethylene tube was inserted into the efferent limb to study small intestinal contractions using low compliance pneumo-hydraulic water-perfused manometry. Octreotide acetate prevented dumping symptoms in all six patients and induced the appearance of migrating myoelectric complexes (MMC) characteristic of interdigestive motility. After ingestion of the dumping meal the postprandial "fed" motility pattern lasted for 141 +/- 9 min while after octreotide acetate the fed motility lasted for 29 +/- 5 min (P less than 0.03). The vigor of the fed motility pattern as measured by the motility index (MI = loge (sum of amplitudes X No. of contractions + 1] was lower after octreotide acetate than after placebo (15.1 +/- 0.1 vs 13.4 +/- 0.2, P less than 0.03). The induction of fasting MMC motility pattern and reduction in the duration and vigor of fed motility may explain the symptomatic relief these patients obtained with octreotide acetate. It is not known whether the induction of the MMC is a direct effect of octreotide acetate or secondary to the concomitant inhibition of peptide release (neurotensin, insulin, glucagon, pancreatic polypeptide) that has been demonstrated in earlier studies.
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PMID:Octreotide acetate induces fasting small bowel motility in patients with dumping syndrome. 226 84

Octreotide acetate (Sandostatin), a long-acting somatostatin analogue, has been demonstrated to inhibit pancreatic exocrine secretion. The effect of octreotide acetate on pancreatic endocrine function in patients undergoing pancreas surgery or pancreas transplantation has not been as well described, nor have the clinical implications been studied as systematically. This study was designed to investigate the effects of octreotide acetate on glucose metabolism and endocrine function in a partial pancreatectomized canine model, simulating reduced islet cell reserve. Serum levels of glucose, insulin, and glucagon were determined at intervals over 2 hr following an intravenous glucose tolerance test (0.5 g/kg intravenous bolus of 50% glucose) in: normal animals (Group A, n = 5), normal animals pretreated with an intravenous bolus of 400 micrograms of octreotide acetate (Group B, n = 5), partial pancreatectomized animals (Group C, n = 5), and partial pancreatectomized animals pretreated with an intravenous bolus of 400 micrograms of octreotide acetate (Group D, n = 5). Peak glucose concentration was significantly increased in Group D when compared to Group C (Group C = 304.2 +/- 13.5 mg/dl vs Group D = 353.2 +/- 12.9 mg/dl, P < 0.05), indicating an impairment of glucose metabolism by octreotide. In addition, octreotide significantly decreased peak insulin release in the partial pancreatectomy groups (Group C = 129 +/- 12.9 micro U/ml vs Group D = 47.5 +/- 6.8 micro U/ml, P < 0.05). There were no significant differences in the rate of glucose utilization or glucagon concentrations among the groups. These results demonstrate that octreotide does result in insulin suppression, with a resultant increase in stimulated glucose concentrations, in a canine model of reduced islet cell mass. Further studies are required to determine the mechanism of action of octreotide on endocrine function in the setting of pancreas transplant.
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PMID:Effect of octreotide on pancreatic endocrine function in partial pancreatectomy. 865 23

Somatostatin analogues are potent growth hormone and glucagon inhibitors and are commonly used in the treatment of several endocrine and non-endocrine disorders. We report severe and longstanding hypoglycemia triggered by long-acting octreotide (Sandostatin LAR) in a 62-year-old women with malignant mesenchymal tumor. Hypoglycemia developed after 6 hours of octreotide injection and she was admitted to the emergency unit with sweating, tremor, palpitation and confusion. On admission, her plasma glucose level was: 17 mg/dl (normal: 65-110), cortisol: 31 microg/dl (normal: 5-25), insulin: 4.32 microIU/ml (normal: 6-27), C-peptide: 2.64 ng/ml (normal: 0.9-4.0), growth hormone: 0.06 ng/ml (normal: 0.06-5.0), insulin-like growth factor-I: 8.5 ng/ml (normal: 101-303), insulin-like growth factor binding protein-3: 1715 ng/ml (normal: 2020-3990). Intravenous dextrose infusion was given for a month to sustain normoglycemia since hypoglycemia recurred following cessation of infusion. Therefore, prednisolone, 35 mg/day was added and the parenteral dextrose infusion rate was decreased gradually and finally stopped. Normoglycemia could be maintained with prednisolone 20 mg/day. In patients prone to tumor hypoglycemia, long-acting octreotide may trigger severe and prolonged hypoglycemia due to suppression of counter-regulatory hormones; clinical trial with short-acting octreotide may be warranted to predict and prevent this life-threating complication.
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PMID:Severe and prolonged hypoglycemia triggered by long-acting octreotide in a patient with malignant mesenchymal tumor: case report. 1267 21