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 12-year-old, 195 kg Shetland pony broodmare had eight seizures between May 29 and August 7, 1979. Plasma glucose levels during three of these seizures were markedly depressed (16, 18 and 19 mg/100 ml). Serum insulin levels were elevated during two of the seizures (86.0 and 97.7 microU/ml). Although a fasting hypoglycemia was not demonstrated, plasma glucose values during a normal day were abnormal; a plasma glucose level of 42 mg/100 ml was noted eight hours post-feeding. Serum insulin values obtained during an oral glucose tolerance test and intravenous glucagon tolerance test were consistent with organic hyperinsulinism of a pancreatic origin. An intravenous glucose tolerance test and a twenty-four hour fast failed to differentiate between the subject and control ponies with respect to plasma glucose and serum insulin levels. Gross and microscopic pathological evaluation of the pancreas revealed a single 2.0 mm adenoma of pancreatic islet cell origin and hyperplasia of islet cells, predominantly beta cells. This is the first report of hypoglycemic seizures in a horse as a result of a pancreatic neoplasm and associated hyperinsulinism.
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PMID:Hypoglycemic seizures in a Shetland pony. 630 51

The diazoxide infusion test (600 mg i.v. over a 1-hour period) was performed in 12 patients bearing single benign islet B-cell adenoma and in 6 normal subjects. Blood glucose, plasma insulin and glucagon concentrations were measured every 15 min during the infusion and thereafter up to 150 min. In insulinoma patients, blood glucose levels failed to increase significantly while in the control group a significant rise starting from 30 min persisted throughout the test (p less than 0.05 or less). Plasma insulin mean levels decreased significantly in normal subjects from 30 to 60 min (p less than 0.05), while they were significantly suppressed in hypoglycemic patients from 15 to 120 min (p less than 0.02). Diazoxide administration induced in the normal group a significant decrease in glucagon levels (p less than 0.02 from 30 to 150 min) whereas no such suppression occurred in patients. In our experience, insulin response to diazoxide infusion in patients with insulinoma may provide additional information for diagnosis.
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PMID:Diazoxide infusion test in patients with single benign insulinoma. 630 33

Clinical and biochemical data are presented on 18 children with severe hyperinsulinaemic hypoglycaemia born to non-diabetic mothers. Thirteen presented within three days of birth, three by 20 months and two aged nine years. Diagnosis of hyperinsulinism (HI) was made in a single blood sample by showing inappropriate plasma insulin levels (23 +/- 3 mU/l) for glycaemia (1.2 +/- 0.1 mmol/l), with low blood ketone body, lactate, alanine and glycerol levels. All children showed increased glucose disappearance rates (KG 7.6% +/- 0.06) and glucose requirement (range, 9-25 mg/kg/min) and an exaggerated glycaemic response to glucagon when hypoglycaemic. Confirmatory tests included measurement of plasma insulin levels during leucine and arginine tolerance tests, during hypercalcaemia and after fish insulin. Coeliac angiograms were performed in three cases. Clinical progress could be divided into five categories. Four cases recovered normal insulin control spontaneously (transient neonatal HI); two children responded and remain on diazoxide therapy, two responded to diazoxide after partial pancreatectomy (diazoxide responsive HI); in three cases resolution of hypoglycaemia resulted from resection of isolated adenoma (insulinoma); total pancreatectomy was needed in five cases (nesidioblastosis) and two children were victims of drug administration (drug induced HI). This analysis allows the definition of a practical approach to diagnosis and management of this major clinical problem.
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PMID:Hyperinsulinaemic hypoglycaemia in infancy and childhood: a practical approach to diagnosis and medical treatment based on experience of 18 cases. 639 78

We report the histological, ultrastructural, and immunocytochemical features of six hypothalamic gangliocytomas associated with pituitary GH cell adenomas and/or acromegaly. In four patients, the gangliocytoma was intrasellar, and no hypothalamic investigation was performed; in two patients, autopsy confirmed hypothalamic involvement. Four patients had a gangliocytoma associated with pituitary GH cell adenoma and acromegaly; electron microscopy demonstrated an intimate association between neurons and adenomatous GH cells. One patient had a gangliocytoma and a GH cell adenoma but no clinical evidence of acromegaly. In the sixth patient, clinical and biochemical acromegaly was manifest, but no pituitary adenoma was demonstrated. Using immunocytochemistry, human pancreatic tumor GRF (hptGRF-40) was localized in the majority of neurons of all six gangliocytomas. The pituitary adenomas and nontumorous adenohypophyses were negative for hptGRF-40. In addition, somatostatin, glucagon, and GnRH were demonstrated within some neurons of several tumors; insulin and gastrin stains were equivocal. These findings confirm previous proposals of production of a GRF by such gangliocytomas. While the significance of other peptides found in some of the tumors is uncertain, the presence of hptGRF-40 in neurons of these gangliocytomas supports the theory that GRF excess is the mechanism responsible for over-production of GH and provides evidence for a syndrome of hypothalamic acromegaly.
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PMID:A case for hypothalamic acromegaly: a clinicopathological study of six patients with hypothalamic gangliocytomas producing growth hormone-releasing factor. 642 59

Glicentin-containing cells (Glic. cells) in intestinal metaplasia, adenoma and carcinoma of the stomach were examined using immuno-histochemical techniques. Glic. cells first occurred in the gastric mucosa of the transitional area between metaplastic and intact gastric glands. They frequently showed hyperplasia or micronoduli in the budding area of the deeper metaplastic glands, but in completely intestinalized mucosa these endocrine cells decreased remarkably. Gastric adenomas with mild dysplasia had a good number of glicentin-immunoreactive cells which were located in the deeper adenoma glands. Gastrin- and somatostatin-positive cells were also detected in the adenomas. The incidence of glicentin-positive tumor cells was significantly higher in well differentiated adenocarcinoma than in poorly differentiated adenocarcinoma. Among the seven cases of scirrhous argyrophil cell carcinoma, three showed glicentin- and glucagon-immunoreactivity in the same area of the tumor. These findings suggest that the selective increase of Glic. cells in intestinal metaplasia may be closely related to the development of gastric adenoma. Glicentin positive tumor cells in gastric carcinomas can be regarded to be an expression of intestinal or fetal markers.
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PMID:Glicentin-containing cells in intestinal metaplasia, adenoma and carcinoma of the stomach. 643 45

Individuals with type Ia glycogen storage disease (glucose-6-phosphatase deficiency) frequently develop hepatic adenomas. Potential complications involving these adenomas include malignant transformation and hemorrhage. Five of 9 patients with this disease had evidence of hepatic filling defects on radionucleotide liver scan when first evaluated at our hospital. Dietary therapy aimed at preventing hypoglycemia was begun in 7 of the 9 patients. Prevention of hypoglycemia resulted in the correction of all of the metabolic abnormalities (lactic acidosis, hyperlipidemia, hyperuricemia, and growth retardation). Treatment also corrected the marked elevation in plasma glucagon concentrations. A disappearance of the hepatic lesions occurred in 2 of the treated patients, and a marked reduction in size of the adenoma occurred in the third patient. The hepatic filling defects remained present in the two untreated patients. None of the affected patients receiving dietary therapy have developed hepatic adenomas. One of these patients is now 22 yr old and has received dietary therapy for 7 yr. Early dietary therapy seems to be effective in preventing development of adenomas as well as inducing their resolution.
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PMID:Regression of hepatic adenomas in type Ia glycogen storage disease with dietary therapy. 694 8

In a pancreatic adenoma approximately 78.7% of the endocrine cells reacted specifically with antisera to neurotensin, 17.5% to gastrin, 2.8% to pancreatic polypeptide, and 1% to glucagon. The electron microscope revealed that the majority of the endocrine cells were N-cells--morphologically similar to the ileal N-cells which are known to represent the neurotensin-producing cells. Neurotensin was extracted from the tumor and identified by Sephadex, ion-exchange, and high-pressure liquid chromatography. Gastrin, pancreatic polypeptide, and glucagon cells were also identified by the electron microscope; the peptides were extracted and demonstrated by chromatography. The serum concentrations of these hormones were elevated. After total gastrectomy which was necessary because of Zollinger-Ellison syndrome, a jejunoesophageal alkaline reflux, reaching the upper esophagus appeared. As intravenous infusion of synthetic neurotensin in rats caused an increase of luminal enteric pressure, it is suggested that severe jejunoesophageal reflux after gastrectomy may be a clinical feature of a neurotensinoma.
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PMID:A multihormonal tumor of the pancreas producing neurotensin. 730 61

We report the case of a 62-year-old woman who was admitted to our hospital with diabetic ketoacidosis. Her urinary C-peptide was 3.5 micrograms/day, HLA typing was DR9, and serum was positive for islet cell antibodies. There was no significant increase in the major viral titer. Pancreatic head tumor was suspected, and pancreaticoduodenectomy was performed. The pathology of this tumor was polycystic adenoma. We examined the surgical specimen from around the tumor histologically. The pancreatic islets had decreased in number. The immunohistochemical staining of islets for insulin, glucagon and somatostatin showed that the number of B cells had decreased remarkably, while A and D cells were preserved. Marked lymphocytic infiltration was observed in the islets. The majority of lymphocytes were helper/inducer and suppressor/cytotoxic T cells, which did not express HLA-DR antigen or interleukin-2 receptor. No NK cells were present in the islets. The present case, which was examined histologically in detail, is consistent with the previously proposed hypothesis that autoimmunity might play an important role in the pathogenesis of insulin-dependent diabetes mellitus.
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PMID:Type 1 (insulin-dependent) diabetic patient with remarkable infiltration of lymphocytes to the islets. 795 31

From 50 published cases of hepatocellular adenoma (HCA) in glycogen storage disease, type I (GSD I) some characteristic features may be deduced: 1. The male:female ratio was 2:1. This sharply contrasts to HCA of other origin which shows a strong female preponderance. 2. The histology of adenomas largely corresponded to other adenomas, except for the appearance of Mallory bodies, accompanied by neutrophilic inflammation and a peculiar lamellar fibrosis. This observation is of particular interest because Mallory bodies have so far not been described in adenomas but are a well established feature in hepatocellular carcinoma of any aetiology. 3. Adenomas had a tendency to regress after continuous nocturnal intragastric feeding, although not all cases responded favourably. 4. Ten cases of hepatocellular carcinoma (HCC) are recorded in GSD I in literature, whereby in half of them transition from HCA into HCC seems likely. 5. The similarity in clinical presentation and evolution with oestrogen-induced tumours is striking. Pathogenesis of adenoma formation in GSD I is not understood. Experimental evidence and the clinical observation of regression after correction of the metabolic imbalance suggest three possible candidate mechanisms: (1) a glucagon/insulin imbalance; (2) cellular glycogen overload; and (3) proto-oncogene activation. Evidence in favour of these three mechanisms from experimental studies and observations in humans are briefly reviewed.
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PMID:Glycogen storage disease I and hepatocellular tumours. 839 47

Glucagonoma is a rare islet cell tumor of pancreas. Only 122 proven cases have been reported in the English literature so far. Diagnosis of glucagonoma has usually been delayed. The average size of clinically detected glucagonomas was 5.8 cm, and 54.7% of them exhibited metastasis. We describe the case of a 0.7-cm asymptomatic pancreatic glucagonoma. A 45-yr-old female was demonstrated to have a demarcated, small, low echoic mass in the pancreatic head by routine ultrasonography. Table incremental dynamic computed tomography showed a small well-enhanced mass recognized only in an early phase. A 0.7 x 0.7 cm firm nodule on the pancreatic head was excised at operation. Immunohistochemical and ultrastructural studies revealed that this tumor was a glucagon-producing adenoma. This may be the smallest glucagonoma detected by image diagnostics that has been reported in the English literature. Possible early detection of glucagonoma was discussed in this report.
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PMID:Early detection of pancreatic glucagonoma. 854 May 21


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