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)

Four hypercalcemic infantile renal tumors were shown to secrete glucagon-like peptides. These unusual tumors were histologically classified as rhabdoid tumors of the kidney (3 cases) and a cellular mesoblastic nephroma (1 case). Elevated G-29 and G-37 glucagon levels were detected in the plasma and tumor extracts as well as in the supernatants of cultured tumor explants. Three of these tumors were heterotransplanted into the nude mice and serially passaged from a mouse to another. The glucagon level decreased in the transplanted tumor extracts with the number of passage.
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PMID:Ectopic G-29 and G-37 glucagon secretion by hypercalcemic infantile renal tumors. 301 99

The ability of infantile hypercalcemic tumors (three rhabdoid renal tumors, one cellular mesoblastic nephroma, and one hepatoblastoma) to produce parathyroid hormone (PTH) was tested using RNA-DNA hybridization. Results were compared with those obtained in one lung epidermoid carcinoma and one parathyroid adenoma from adult patients. Elevated plasma immunoreactive PTH (iPTH) concentrations were observed in three of five children. The only tumor in which PTH-RNA hybridization could be detected was the parathyroid adenoma. The integrity of the RNA preparations was further confirmed by positive hybridization obtained with a glucagon DNA probe in both normal pancreas and the rhabdoid tumors. Quantitative bone histomorphometry of tumor-bearing nude mice showed a reduction in bone formation and increased bone resorption, the opposite of what occurs in hyperparathyroidism. The PTH-like protein, which was detected by radioimmunoassays (RIA) in the sera of three patients, could not be correlated with tumor PTH mRNA transcription within the limits of our assays. In order to explain this discrepancy, we suggest that the tumors produce a factor (not PTH) which, in turn, elicits the excess iPTH which we detected by RIA.
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PMID:PTH mRNA transcription analysis in infantile tumors associated with hypercalcemia. 338 30

Normal human physiology is dependent on a tight control of the fasting blood glucose (FBG) levels. The islets of pancreas maintains FBG levels within a narrow range of 4-6mmol/L by secreting various hormones, especially insulin and glucagon. However, the hormone secretions by the islets of pancreas are governed by a collective effort among pancreas-islet axis, brain-islet axis, liver-islet axis, gut-islet axis, and adipocyte/myocyte-islet axis. Furthermore, the damage of pancreas, vascular system, brain, liver, intestine, adipose, muscle, and other organs and tissues might affect FBG levels through insulin resistance or impaired insulin signaling, which is the hallmark of type 2 diabetes. In this study, 320,572 clinical lab test results of FBG levels from healthy individuals and patients with 64 different types of diseases during the past 5 years in our hospital were retrieved and analyzed. Based on the mean (SD), median, and p (-Log10p) values, we found 57/64 diseases including type 2 diabetes, pancreatitis, diabetic nephropathy, and pancreatic cancer had significantly (p<0.05, -Log10p>1.30) increased whereas 6/64 diseases including preeclampsia, Wilms' tumor, and lupus erythematous had significantly decreased FBG levels compared to that of healthy controls. These data indicated that the increased FBG levels might be a general pathophysiological property of diseased tissues or organs and the increased FBG levels might be a consequence but not the cause for either prediabetes or type 2 diabetes.
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PMID:Fasting blood glucose levels in patients with different types of diseases. 3090 57