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 purpose of this study was to develop a nonenzymatic method of isolating adult islets using atrophied pancreata from copper-deficient rats and to analyze their morphologic characteristics and behavior in culture. This unusual model of isolation was studied because islets remain intact in the course of dietary copper deficiency while the acinar glandular component of the pancreas undergoes selective atrophy and lipomatosis. Small fragments containing islets were readily microdissected from atrophied glands and placed in culture. Within 24 h the fragments congealed into small irregular- to spherical-shaped masses within which the darker profile of islets could be distinguished. Within a period of 3 to 5 d, islet tissue began to bud from the lipocytic mass until by Day 7 spherical aggregates of intact islet tissue separated from the residual fragments. Subsequent to further in vitro treatment, these islets could be maintained as free viable spherical masses if periodically agitated, as attached stationary islets which developed monolayer growth if left undisturbed and as aggregated masses of islet tissue forming megaislets if combined in small groups. Grouped islets treated with actinomycin D and cycloheximide did not exhibit aggregation when incubated with these inhibitors. This suggests that megaislet formation was an active process requiring protein-RNA synthesis rather than passive clumping or aggregation that can accompany metabolically altered or dying islets undergoing cellular shedding and adhesion. Immunohistochemical localization demonstrated that insulin, glucagon, somatostatin, and pancreatic polypeptide-immunoreactive cell types were present within the islets derived from this technique. The cellular topography of these islets was not unlike that described by others for islets cultured from enzymatic isolation. This culture model may serve as a resource for mature, viable islets isolated without mechanical or enzymatic disaggregation which can have attenuating effects on islet function.
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PMID:Nonenzymatic isolation and culture of adult islets from atrophic pancreata of copper-deficient rats: a morphologic analysis. 289 82

A modification of a technique to isolate kidney tubule fragments and pancreatic acinar cells has been used to prepare a suspension of pancreatic duct fragments from rats with pancreatic lipomatosis due to pretreatment with penicillamine and a copper-free diet. This suspension is 90-95% pure almost without any acinar cell contamination. The accumulation of 3',5'-cyclic adenosine monophosphate (cAMP) in response to various gastrointestinal hormones, hormone-like substances and theophylline was studied in these isolated pancreatic duct fragments. In the absence of theophylline, secretin increased the level of cAMP in a dose-dependent manner with a maximum at 10(-6) M. With supramaximal doses the concentration of cAMP decreased. During maximal stimulation with secretin the level of cAMP was dependent on the concentration of fragments in the incubation mixture. Vasoactive intestinal peptide (VIP) also increased the formation of cAMP. However, VIP was 10 times less effective than secretin on a molar basis. The addition of various concentrations of VIP to a submaximal dose of secretin did not alter cAMP levels as compared to the levels observed with the same concentration of secretin alone. Theophylline (5 x 10(-3) and 10(-2) M) stimulated cAMP accumulation and 5 x 10(-3) M theophylline potentiated the response to secretin and VIP. Pancreozymin (20 and 99% pure), glucagon bovine pancreatic polypeptide and carbamylcholine did not effect the level of cAMP when given alone or in combination with secretin. These data lend support to the hypothesis that cAMP is the intracellular mediator of the action of secretin and VIP on the pancreatic duct cells.
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PMID:Effects of gastrointestinal hormones and carbamylcholine on cAMP accumulation in isolated pancreatic duct fragments from the rat. 624 7

Multiple Symmetric Lipomatosis (MSL) is a syndrome characterized by the occurrence of symmetric lipomas over various regions of the body. No clear etiology has been recognized while a frequent association with systemic metabolic abnormalities has been described. The metabolic situation of a subject affected by MSL was assessed before and after surgical excision of lipomas. A condition of impaired glucose tolerance (IGT) was verified both before and after surgery by the performance of oral glucose tolerance test, glucagon test, and daily glucose profile. No significant differences were observed after the ablation of lipomatous masses with regard to glucose, IRI, IRCP and NEFA behaviour. We concluded that the resection of lipomas can not modify glucose tolerance in MSL and that lipomas can be considered as tissues metabolically independent from the rest of body fat.
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PMID:[Multiple symmetrical lipomatosis. Metabolic effects of excision of lipomatous tissue]. 815 30

Five callitrichids (three common marmosets -Callithrix jacchus -, a black tufted-eared marmoset -C. penicillata-, and a saddle-back tamarin -Saguinus fuscicollis) were diagnosed with islet hyperplasia by histopathology and immunohistochemistry. All were privately-owned, unrelated callitrichids ranging from 2- to 4-year-old. Relevant findings were anorexia (3/5), vomiting (2/5), ptyalism (1/5), polyuria/polydipsia (1/5), respiratory distress (1/5), hyperglycemia (2/3) and glycosuria (1/1); hyperglycemia and glycosuria were associated with pregnancy in a common marmoset and resolved after reducing simple carbohydrates in diet. All five animals died, three of them after few premonitory signs; in two cases, other concurrent diseases unrelated to islet hyperplasia were considered the cause of death. Additional animals from two facilities had high weight (4), physical obesity (3), polyuria/polydipsia/polyphagia/uriposia (1), hyperglycemia (1), and/or glycosuria (2). Pathologic findings in the deceased callitrichids were: islet hyperplasia (5/5); hemosiderosis (5/5); lipomatosis (4/5) of several tissues (atria, 3/5; pancreas, gall bladder, intestine, esophagus, and thyroid, 2/5; liver, 1/5); pancreatic necrosis or steatonecrosis, and/or acute pancreatitis (3/5); and vacuolation of hepatocytes and renal tubular cells most likely consistent with hepatorenal lipidosis (2/5). The islets of Langerhans were more numerous and larger than in a control, and morphologically normal in all cases, except in a common marmoset that had a few cells with a foamy cytoplasm and shrunken hyperchromatic or picknotic nucleus. Insulin (5/5), glucagon (3/5), and somatostatin (3/5) immunohistochemistry revealed that most cells stained positively for insulin diffusely in their cytoplasm (5/5) (staining restricted to the vascular pole of b-cells in the control). These findings suggest that obesity, insulin resistance and/or type II diabetes may be implicated and thus a prospective study on these diseases in callitrichids is necessary to determine their etiopathogenesis.
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PMID:Islet hyperplasia in callitrichids. 1214 99

A 12-year-old neutered female mixed-breed dog was referred for occasional vomiting that had increased progressively in frequency over the past 3 months. Palpation of the abdomen revealed a firm mass of unknown aetiology, located within the cranial to mid abdomen, while abdominal surgical exploration revealed a well-defined abdominal mass of pancreatic origin. The pancreatic mass caused lateral displacement of the duodenum as well as medial displacement of the pylorus, resulting in impairment of pyloric outflow. Further examination revealed a firm, poorly vascularized and coarsely lobulated structure. The histopathological findings were consistent with severe pancreatic lipomatosis and atrophy. Immunohistochemically, the remnant pancreatic cells were positive for cytokeratins AE1/AE3 and glucagon, and negative for insulin. Routine follow-up with the referring veterinarian showed no evidence of postoperative complications, but the dog continued to deteriorate further and died despite medical management. Pancreatic lipomatosis is a rare condition in small animal practice. The aetiology or predisposing factors have not been identified in animals.
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PMID:Extensive Fatty Replacement of the Pancreas (Pancreatic Lipomatosis) in a Dog. 3181 69