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)

A 53 year old woman presented with diabetes mellitus, hyperglucagonemia (600 to 1,500 pg/ml), clinical hyperparathyroidism and an abdominal mass diagnosed on biopsy as an islet cell carcinoma. Glucagon content of the tumor was 0.78 mug/g wet weight. Hourly blood samples during a 24 hour period revealed a direct correlation between plasma glucose and glucagon. The oral administration of glucose paradoxically increased whereas the intravenous administration decreased plasma glucagon. Circulating glucagon levels were markedly increased with arginine and epinephrine infusion. Both short- and long-term administration of alpha adrenergic blockade depressed the glucagon response to epinephrine infusion. In contrast, long-term alpha adrenergic blockade increased glucagon secretion despite improved glucose tolerance during a second 24 hour study. Although the patient demonstrated overt clinical and chemical findings of hyperparathyroidism, parathyroid hormone (PTH) was not detected in her plasma. The pattern of tumor growth was consistent with an origin from pancreatic islets. We conclude that (1) the tumor was responsive to physiologic stimuli known to affect glucagon secretion; (2) elevations of plasma glucagon levels with oral and dietary glucose suggest regulation of secretion by intestinal factors; and (3) improvement of glucose tolerance with alpha adrenergic blockade may be related to increased insulin secretion.
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PMID:Uncontrolled diabetes mellitus and hyperglucagonemia associated with an islet cell carcinoma. 4 4

To elucidate pathogenetic factors of bone mineral loss in diabetes mellitus, bone mineral content (BMC), glucose and calcium homeostasis were evaluated in a cross-sectionsl study of 215 insulin-treated diabetics. BMC declined 10% during the first 5 years of diabetes. This coincided with cessation of insulin secretion, deterioration of metabolic control and raising urinary calcium excretion rates of calcium and phosphorus. BMC was inversely correlated to fasting blood glucose (P less than 0.02), to glycosuria (P less than 0.02) and to insulin requirement (P less than 0.002), and positively to the glucagon-stimulated serum C-peptide levels (P less than 0.005). Urinary excretion rates of calcium and phosphorus correlated positively with the degree of hyperglycaemia (P less than 0.001) and glycosuria (P less than 0.001). The skeletal calcium loss corresponded to the excess of urinary excretion during the phase of BMC reduction. There was no evidence of secondary hyperparathyroidism. The relationship between bone loss and disturbed glucose homeostasis indicates that diabetic bone loss is secondary to the metabolic abnormalities, possibly acting directly on bone.
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PMID:Bone mineral loss in insulin-treated diabetes mellitus: studies on pathogenesis. 42 86

Plasma glucose, insulin, and alpha-cell glucagon profiles were examined in ten adults with uncomplicated primary hyperparathyroidism before and 8-12 week after surgical removal of a single parathyroid adenoma. Treatment restored abnormal serum calcium and phosphorus concentrations to a normal range and reduced serum parathyroid hormone levels from 47 +/- 4 to 16 +/- 4 mu 1 Eq/ml (normal = 0-40). Plasma glucose curves during 100-g oral glucose tolerance, 30 min intravenous glucose (1.5 g/min), or arginine infusions (1.0 g/min) did not differ before and after surgery. However, basal and peak insulin concentrations were higher before treatment during these tests (p less than 0.05). Basal glucagon levels were unaffected by hyperparathyroidism (72 +/- 7 versus 77 +/- 7 pg/ml). Peak 30 min values after arginine provocation were also similar before and after treatment as was maximal suppression of basal glucagon during glucose infusions. Four patients also received 400 g lean beef meals. Glucose and glucagon responses over 240-min periods were nearly identical before and after surgery despite higher insulin levels before treatment. It is concluded that elevated serum parathyroid hormone and plasma insulin concentrations in primary hyperparathyroidism do not relate to abnormalities of plasma alpha-cell glucagon in the basal state or after glucose, arginine, or protein administration.
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PMID:Plasma alpha-cell glucagon in primary hyperparathyroidism. 78 68

An adequate therapy must be directed towards the cause of the recurrent ulcer. This is incomplete vagotomy in most cases, more seldom a hypergastrinemia with stasis in the antrum after insufficient drainage, in hyperparathyroidism, in hyperplasia of the antral G cells or in gastrinoma. After confirmation of the diagnosis by endoscopy, a causal diagnosis must therefore be made which includes secretion analysis and determination of the gastrin profile (feeding test, glucagon provocation test, secretion or calcium infusion). Criteria for evaluation and clinical conclusiveness are shown in examples. The indication scheme, whether revagotomy alone, resection alone or the combination of the two corrective operations should be performed is determined according to these criteria. So far, 41 patients have been operated on with good results in accordance with this graduated indication.
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PMID:[Recurrent ulcer following vagotomy: completion of vagotomy or resection (author's transl)]. 81 80

A 42-year-old woman with a family history of multiple endocrine neoplasia type 1 (MEN 1) presented with symptomatic hypoglycaemia and peptic ulceration. Investigation revealed an insulinoma, hyperparathyroidism, hypercalcitoninaemia with a positive pentagastrin stimulation test, acromegaly due to a GRF-oma, hyperprolactinaemia and normal serum gastrin levels. Five pancreatic tumours were removed at laparotomy and immunostaining was positive for insulin, calcitonin, somatostatin and glucagon. Post-operatively she developed elevated serum gastrin levels and gross peptic ulceration, despite H2-blockers, and died of gastro-intestinal haemorrhage suggesting that removal of the somatostatinoma may have allowed increased gastrin secretion from a gastrinoma. This case emphasizes the importance of measuring a wide variety of tumour marker peptides in MEN 1 and suggests that caution is required in interpretation of the pentagastrin stimulation test in such cases. Patients with MEN 1 and known peptic ulceration may require perioperative omeprazole treatment even if serum gastrin levels are normal.
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PMID:A case of multiple endocrine neoplasia: hyperparathyroidism, insulinoma, GRF-oma, hypercalcitoninaemia and intractable peptic ulceration. 135 65

This study was designed to investigate pancreatic exocrine and endocrine secretion stimulated with secretin and thyrotropin-releasing hormone (TRH) in hyperparathyroidism. Pancreatic exocrine secretion during 30 min stimulated by constant secretin infusion of 1U/kg/hour was significantly increased in patients with secondary hyperparathyroidism compared with controls and patients with primary hyperparathyroidism. Intravenous administration of TRH at a dose of 20 micrograms/kg/hour, superimposed on secretin, produced a significant decrease of pancreatic exocrine secretion in both primary and secondary hyperparathyroidism but not in control. Serum insulin, glucagon and secretin levels were significantly higher in the subjects of both primary and secondary hyperparathyroidism than those of controls. Serum glucagon and secretin levels were significantly higher in secondary hyperparathyroidism than primary hyperparathyroidism. The pancreatic endocrine secretion was not influenced by TRH administration. Pancreatic exocrine secretion was not changed by parathyroidectomy in patients with primary hyperparathyroidism. As for endocrine secretion, however, only serum secretin level decreased to the level before parathyroidectomy. In this study, it was speculated that the increase of pancreatic secretion in secondary hyperparathyroidism may be due to hypersecretinemia, and the decrease of exocrine secretion by TRH in primary and secondary hyperparathyroidism may be resulted from the direct effect of TRH on the pancreatic acinar cells.
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PMID:[Pancreatic exocrine and endocrine functions stimulated with secretin and thyrotropin-releasing hormone in patients with hyperparathyroidism]. 137 24

A total of 79 consecutive patients with pituitary tumours were screened for multiple endocrine neoplasia type 1 (MEN-1). The 79 patients included 21 patients with acromegaly, nine with Cushing's disease, 18 with prolactinomas, three with mixed pituitary adenomas (GH and PRL), and 28 patients with no detectable hypersecretion of hormones. The screening consisted of: (1) a family history, (2) a uniform medical history of the patient using a standard questionnaire, and (3) hormonal evaluation including measurements of the serum levels of insulin, gastrin, glucagon, somatostatin, vasoactive intestinal polypeptide and pancreatic polypeptide. Ionized calcium and glucose concentration in serum were also measured. We found no patients with the MEN-1 syndrome. In one patient, we found a transient elevation of serum concentrations of pancreatic polypeptide for which we have no explanation. In another patient, the serum gastrin concentration was elevated secondary to achlorhydria. No other endocrine disorders were found, and no patients had relatives with recognized endocrine pancreatic tumours, primary hyperparathyroidism (HPT), or pituitary adenomas.
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PMID:Screening for multiple endocrine neoplasia type 1 in patients with recognized pituitary adenoma. 198 64

Derangements in leukocyte function occur in patients with primary hyperparathyroidism and in those with uremia, which is a state of secondary hyperparathyroidism, suggesting that parathyroid hormone (PTH) may affect leukocyte function. We examined the interaction between PTH and random migration of human polymorphonuclear leukocytes (PMNL) utilizing a modified Boyden chamber. Intact 1-84 PTH but not its amino-terminal (1-34 PTH) or its carboxy-terminal (53-84 PTH) fragments produced marked and significant (p less than 0.01) stimulation of random migration in a dose-dependent manner. Inactivation of 1-84 PTH abolished its effect and other peptide hormones (calcitonin, glucagon, insulin and vasopressin) did not stimulate migration of PMNL. The effect of PTH on migration was not due to action of the hormone on chemotaxis. PTH did not enhance cAMP or cGMP production by PMNL. The stimulation of PMNL motility by PTH was independent of calcium concentration in media, was not mimicked by calcium ionophore and was not blocked by verapamil. Quinidine also produced significant (p less than 0.01) increase in random migration of PMNL and this effect was not additive to that of PTH. Prolonged exposure to PTH (16-20 h) was associated with significant inhibition of random migration of PMNL. The migration of PMNL from patients with advanced renal failure was significantly (p less than 0.01) reduced and there was a significant (p less than 0.01) inverse relationship between random migration of PMNL and serum levels of PTH. Also PTH produced only modest stimulation of random migration of PMNL in most patients with renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of parathyroid hormone on random migration of human polymorphonuclear leukocytes. 285 73

A case of carcinoid tumor of the pancreas with the watery diarrhea, hypokalemia, and hypochlorhydria syndrome in association with hyperparathyroidism and the amenorrhea-galactorrhea syndrome is presented. Resection of the three grossly enlarged, hyperplastic parathyroid glands restored eucalcemia in this patient. A subsequent excision of the 370 gm pancreatic carcinoid tumor resulted in a cure of the watery diarrhea and a return of the gastric acid secretion to normal. Immunocytochemical studies of the pancreatic tumor demonstrated a positive stain only for serotonin, and negative results for vasoactive intestinal polypeptide, pancreatic polypeptide, glucagon, insulin, cholecystokinin, gastrin, and calcitonin were obtained. These studies suggest that in this patient, serotonin was a causative agent of the watery diarrhea syndrome.
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PMID:Carcinoid tumor of the pancreas causing the diarrheogenic syndrome: report of a case combined with multiple endocrine neoplasia, type I. 286 11

We report the first documentation of GHRH production by a tumour associated with proven multiple endocrine neoplasia (MEN). A 30-year-old woman had hypoglycaemia, hyperparathyroidism, and pituitary adenoma with hyperprolactinaemia. Serum growth hormone elevation was attributed to hypoglycaemia but plasma GHRH was elevated. Subtotal pancreatectomy revealed multiple endocrine tumours and nesidioblastosis. Immunohistochemistry demonstrated insulin, glucagon, and somatostatin in several tumours. GHRH was localized in the largest one and was released from that tumour in vitro. Post-operative plasma GH returned to normal. Excess secretion of humoural factors by one tumour may stimulate growth of other tumours in MEN syndromes. The prevalence of GHRH in MEN-I tumours remains to be established.
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PMID:Pancreatic endocrine tumour producing growth hormone-releasing hormone associated with multiple endocrine neoplasia type I syndrome. 288 80


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