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 effect of cyclic somatostatin on early and late dumping syndrome was studied in 12 patients with gastric resection. Each patient underwent two glucose challenges with 75 grams of glucose administered orally. In the control study isotonic sodium chloride was given, while in the other study cyclic somatostatin in a dose of 250 micrograms bolus injection followed by infusion of 80 ng/kg/min for a period of 270 minutes. In the control study all patients showed subjective symptoms of the early dumping syndrome with significant increases in pulse rate, hematocrit, and vasoactive intestinal polypeptide. Ten patients showed asymptomatic hypoglycemia, as a sign of the late dumping syndrome associated with a significant increases of insulin, gastric inhibitory peptide and glucagon levels. During the administration of somatostatin these changes failed to develop. These results indicate that somatostatin alleviates the symptoms of early and late postprandial dumping syndrome.
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PMID:[The effect of somatostatin in dumping syndrome]. 197 48

The present study evaluates the acute and chronic use of a long-acting somatostatin analog, octreotide acetate, in the treatment of patients with severe postgastrectomy dumping syndrome. In the acute phase, 10 patients with severe dumping were studied over 2 consecutive days before and for 3 hours after the ingestion of a 'dumping breakfast' in a randomized double-blind fashion. On one day octreotide (100 micrograms) was given subcutaneously 30 minutes before the test meal and on the other day an equal volume of vehicle was injected. An additional group of six postgastrectomy patients without dumping were studied in a similar fashion and these acted as controls. During placebo treatment the test meal resulted in an immediate increase (p less than 0.01) in the pulse rate and in plasma levels of glucose, glucagon, pancreatic polypeptide, neurotensin, and insulin. Similar changes were seen in the control group with respect to placebo; however glucagon and neurotensin (p less than 0.05) did not show the same magnitude of increase as seen with placebo. Treatment with octreotide acetate prevented the development of both vasomotor and gastrointestinal symptoms and completely ablated all of the above responses in plasma peptides. These changes were associated with complete ablation of diarrhea (p less than 0.001). Pretreatment with octreotide acetate completely suppressed the rise in plasma insulin response to the meal and this ablated the late hypoglycemia of dumping. Treatment with octreotide acetate resulted in delayed gastric emptying and transit time (578 +/- 244 minutes) versus 76 +/- 23 minutes with placebo and 125 +/- 36 minutes in controls (p less than 0.05). Chronic daily treatment with octreotide acetate resulted in minimal side effects. These patients demonstrated a stable fasting plasma glucose, normal liver function tests, and an average weight gain of 11% during a 12-month period. In addition most patients were able to resume employment. The long-acting somatostatin analog, octreotide acetate, is highly effective in preventing the development of symptoms of severe dumping syndrome, both vasomotor and gastrointestinal.
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PMID:Efficacy of octreotide acetate in treatment of severe postgastrectomy dumping syndrome. 225 59

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

This study was planned in pursuit of the relation between glucagon responses to glucose and the late dumping syndrome. Clinically, 75 g oral glucose tolerance test to seven late dumpers, ten gastrectomized patients and ten normal subjects were performed. And experimentary, 20 ml 25% glucose was put into small intestinal blind loops prepared in dogs, which were made the jejunum region and then the ileum region. 1. The mean oral glucose tolerance curve in gastrectomized patients was oxyhyperglycemic, and this tendency was seen in late dumpers. But, for only late dumpers, the low blood glucose concentration which was under 50 mg/dl appeared within one and half to three hours after oral glucose load. 2. The change of serum IRI in gastrectomized patients displayed the initial hyperinsulinemia, that was similar in late dumpers. 3. Pancreatic glucagon (GI) levels were within normal limits in normal subjects and late dumpers, but were significantly increased in gastrectomized patients. 4. Enteroglucagon (gutGLI) levels were not so increased in normal subjects, but were significantly increased in gastrectomized patients and late dumpers as well. 5. GutGLI levels were increased only by putting into the ileum loop. But hypersecretion of gutGLI did not affect the blood glucose curve and the change of serum IRI significantly. These results described above suggest that the pathogenesis of the hypoglycemia in the late dumping syndrome may be responsible for no hypersecretion of GI, for some reason, to prevent hypoglycemia against hyperinsulinemia with oxyhyperglycemia, and that gutGLI may not play so important part in the regulation of the blood glucose level.
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PMID:[Studies on the relation between late dumping syndrome and glucagon responses to glucose]. 307 47

Three children with severe hypoglycemic reactions secondary to dumping syndrome were studied to discern the mechanism by which hypoglycemia occurred. Symptoms in patient 1 developed after fundoplication, generalized autonomic dysfunction occurred in patient 2, and dumping syndrome developed in patient 3 after malplacement of a feeding gastrostomy tube. Average blood glucose levels studied during and after two to seven meals in each child were 375 +/- 97 mg/dL (mean +/- SD) 30 minutes postprandially and 35 +/- 10 mg/dL greater than 120 minutes later. Swings in glucose values were proportional to the volume of meals. Insulin and glucagon levels were followed during a single meal challenge test in each patient; the average glucose concentration increased to 356 +/- 59 mg/dL 30 minutes postprandially and decreased to 32 +/- 11 mg/dL at 150 +/- 30 minutes. Hormonal analyses indicated (1) inappropriate early release of glucagon (300 pg/mL at 15 minutes) in patient 1, (2) exuberant early release of insulin (maximum 190 +/- 15 microU/mL) resulting in rapid decrease in glucose concentration in all patients, (3) development and/or persistence of hypoglycemia after the decline in circulating insulin to undetectable levels, and (4) inadequate glucagon response to hypoglycemia resulting in sustained hypoglycemia. These data indicate that gross disturbances of the insulin-glucagon axis attend childhood dumping syndrome.
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PMID:Hypoglycemia pathogenesis in children with dumping syndrome. 331 64

To investigate the pathophysiological relation between releases of gut hormones and dumping syndrome, plasma radioimmunoassayable neurotensin, substance P, glucagon-like immunoreactivity (GLI), insulin and blood sugar were measured in both gastrectomized patients and control subjects after 50 g oral glucose tolerance tests. Remarkable rises of radioimmunoassayable neurotensin and GLI were found in all gastrectomized patients, but not in control subjects. In contrast, plasma radioimmunoassayable substance P responses were not detected in either gastrectomized patients or control subjects. There were three patients with symptoms of dumping syndrome in the early stage of the test. Plasma radioimmunoassayable neurotensin responses in two out of these three were higher than those in other patients, though the other patient with symptoms had the same degree of neurotensin elevation as patients with no symptoms. In view of the pharmacological effects of neurotensin, it could not be ruled out that a part of the early symptoms of dumping syndrome may result from the remarkably enhanced plasma neurotensin release in some patients, although the enhanced neurotensin responses did not always accompany symptoms of dumping syndrome.
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PMID:Neurotensin and substance P and dumping syndrome. 617 87

A means of estimating human enteroglucagon (glucagon-like immunoreactivity of intestinal origin) in tissues and plasma is described, based on the subtraction of RIA values obtained with the C-terminal-directed glucagon antiserum RCS5 from the total glucagon-like immunoreactivity determined with the N-terminal- to midmolecule-directed glucagon antiserum R59. Gel filtration on Sephadex G-50 of human plasma and extracts of normal human intestine separated the R59 immunoreactivity into three peaks: a small peak of void volume material, a major peak coeluting with porcine glicentin, and a smaller peak coeluting with pancreatic glucagon. No RCS5 immunoreactivity was detected in the human gut, except for a small amount constituting less than 2% of the total glucagon-like immunoreactivity in the ileum and rectum only. In extracts of human pancreas, the chromatographic profiles obtained with RCS5 and R59 assays differed from the intestinal patterns, but were identical to each other, giving no evidence of a significant amount of pancreatic R59 immunoreactivity that was not also reactive with RCS5. Chromatography of plasmas from healthy subjects and patients with dumping syndrome, active coeliac disease, and tropical sprue showed that only the second major peak of R59 immunoreactivity reflected the basal or postnutrient increases in the plasma enteroglucagon concentration. In patients with exaggerated enteroglucagon release, the rise was again found to be entirely due to an increase in this peak of immunoreactivity. This major molecular form of human enteroglucagon, similar in size to porcine glicentin, is, thus, the form most likely to be of physiological and pathophysiological significance.
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PMID:Molecular forms of human enteroglucagon in tissue and plasma: plasma responses to nutrient stimuli in health and in disorders of the upper gastrointestinal tract. 687 88

The secretion of hormones stimulating and inhibiting gastric secretory activity was studied in 85 patients with postvagotomy syndromes. The somatropin level was found to increase significantly in gastrostasis. The lower values of the blood insulin and C-peptide content in patients with recurrent ulcers was evidently associated either with insufficiency of the pancreatic insular apparatus or with partial vagal denervation, increased STH level, and plausible inhibiting effect of glucagon. Increased somatostatin secretion in the dumping syndrome, gastrostasis, and peptic ulcers may be due to the encountered hypergastrinemia.
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PMID:[Neurohumoral regulation of gastric secretion in postvagotomy syndromes]. 793 83

The effect of somatostatin on early and late dumping syndrome was studied in 12 patients with gastric resection. Each patient underwent two glucose challenges with 75 gram of glucose administered orally. In the control study isotonic sodium chloride was given, while in the other study cyclic somatostatin in a dose of 80 ng/kg/min was given for a period of 270 minutes. In the control study all patients showed subjective symptoms of the early dumping syndrome with significant (p < 0.001) increases in pulse rate, hematocrit, and vasoactive intestinal polypeptide. Ten patients showed asymptomatic hypoglycemia, as a sign of the late dumping syndrome associated with a significant (p < 0.001) increase of insulin, gastric inhibitory peptide and glucagon levels. During the administration of somatostatin these changes failed to develop. The difference between the results of the two challenges are significant. These results indicate that somatostatin alleviates the symptoms both of early and late dumping syndrome partly by inhibiting the vasoactive intestinal polypeptide, gastric inhibitory peptide and insulin release, which are increased in dumping syndrome and may, therefore, be implicated as to have an etiological role.
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PMID:The effect of somatostatin in dumping syndrome after gastric surgery. 810 15

The dumping syndrome is encountered in approximately 10% of patients after gastric surgery. A postprandial peripheral and splanchnic vasodilatation and ensuing relative hypovolaemia are pivotal in the pathophysiology of early systemic symptoms. Late dumping symptoms are a consequence of a reactive hypoglycaemia, which results from an exaggerated insulin and glucagon-like peptide-1 release. The diagnosis of dumping syndrome can reliably be made with the aid of a provocation test using 50 g glucose orally. Most patients with dumping can be treated with advice on diet and lifestyle. Octreotide effectively controls the signs and symptoms of dumping in patients refractory to standard therapy. It acts through its inhibitory effects on insulin and gut hormone release, a delay of intestinal transit time and inhibition of food-induced circulatory changes. Its long-term use is somewhat limited by side effects, particularly diarrhoea and steatorrhoea.
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PMID:The dumping syndrome. Current insights into pathophysiology, diagnosis and treatment. 920 Mar 2


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