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 diabetic state that is seen at a high frequency in association with pancreatic cancer is characterized by elevated plasma levels of several islet hormones and by marked insulin resistance. Both the diabetic state and insulin sensitivity improve after tumor removal by sub-total pancreatectomy. Impaired glucose tolerance has also been found in the hamster pancreatic cancer model, but conflicting data regarding islet function have been reported. In order to further investigate islet function and secretion during early development of pancreatic cancer, we measured the concentrations of insulin, glucagon, somatostatin, and islet amyloid polypeptide (IAPP) in plasma, pancreatic tissue, and secretin-stimulated pancreatic juice at 12 and 27 weeks after the ductal-cell-specific carcinogen, BOP had been used to induce tumors in Syrian golden hamsters. At 12 weeks after BOP, plasma glucagon levels were significantly increased. An exaggerated plasma-glucose response and concomitant hyperinsulinemia were observed at 27 but not 12 weeks after BOP. Plasma IAPP concentrations, but not glucagon or somatostatin, were elevated at 27 weeks. Tissue concentrations of IAPP were substantially reduced in BOP-treated hamsters at 27 weeks. No differences in hormone concentrations were seen in pancreatic juice from the two groups at either of the two time points investigated. The study showed that islet hormone changes accompany the early development of pancreatic tumors in the hamster pancreatic model. The hormone changes and apparent insulin resistance resemble the metabolic changes found in humans with pancreatic cancer.
Teratog Carcinog Mutagen 2001
PMID:Early changes in islet hormone secretion in the hamster pancreatic cancer model. 1113 21

Abnormal glucose tolerance and frank diabetes mellitus develop in up to 80% of pancreatic cancer patients. Islets within these tumors show a decreased number of beta cells and increased number of alpha cells. The reduced number of beta cells could induce beta cell neogenesis in extrainsular tissue to compensate for the loss of insulin in islets. On the other hand, because the beta cell depletion in pancreatic cancer seems to be the effect of substances released by cancer cells, suppression of extrainsular endocrine cells is expected. We compared the pattern of extrainsular endocrine cells in pancreatic cancer patients with normal pancreas as well as chronic pancreatitis, which is known to be associated with impaired glucose tolerance or frank diabetes. As in the normal tissue, extrainsular endocrine cells were found in chronic pancreatitis and pancreatic cancer. However, in the chronic pancreatitis specimens insulin cells were the predominant cell type, whereas in pancreatic cancer specimens more glucagon than insulin cells were found, although the differences were statistically insignificant. Thus, our results indicate that the alteration of beta cells in pancreatic cancer patients is mainly restricted to the endocrine cells within the islets and that there is no compensatory proliferation of beta cells.
Teratog Carcinog Mutagen 2001
PMID:The patterns of extrainsular endocrine cells in pancreatic cancer. 1113 22