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)

Recent data seem to support a tubular defect as the mechanism of the elevated renal clearance of amylase relative to creatinine in acute pancreatitis. Glucagon has been proposed by some to be an important factor in this phenomenon. To examine the role of glucagon as this "tubular dysfunction factor", we investigated the effect of intravenously infused glucagon on the fractional excretion of amylase and the tubular handling of a low molecular weight protein, beta2 microglobulin, in normal, healthy volunteers. At glucagon levels far in excess of those seen in pancreatitis, the clearance ratio of beta2 microglobulin relative to creatinine increased, whereas the clearance ratio of amylase relative to creatinine did not increase above the normal range. The dissociation between beta2 microglobulin clearance and amylase clearance allows one to question the theory that tubular dysfunction is the mechanism of the elevated renal clearance of amylase relative to creatinine in acute pancreatitis. Glucagon does not appear to be the sole factor responsible for the elevation of renal clearance of amylase relative to creatinine in acute pancreatitis.
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PMID:Effect of glucagon infusion on the renal clearance of amylase relative to creatinine. 8 90

A 53-year-old white woman developed diabetes mellitus, migratory erythema, and anemia, clinical features suggesting the presence of a "glucagonoma." Ten years earlier, after laparotomy and pancreatic biopsy, she had been told that she had an inoperable pancreatic carcinoma. Review of that biopsy together with current hormonal assay now confirms the diagnosis of glucagonoma. The recurrent peptic ulcer in this patient despite high levels of glucagon, a gastric inhibitory agent, is noted but not explained. An enhanced amylase-creatinine clearance ratio supports the notion that glucagon increases the clearances of amylase.
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PMID:Glucagonoma, chronic recurrent peptic ulcer disease, and enhanced amylase-creatinine clearance ratio. Report of a case with review of the literature. 9 10

The urinary excretion of cyclic adenosine 3',5'-monophosphate (cAMP), corrected for urinary creatinine, was determined in 177 patients with primary or metastatic tumours and in 149 normal subjects. In 26 patients with malignancy and in 10 control subjects the excretion of cyclic guanosine 3',5'-monophosphate (cGMP) was also evaluated. The urinary cAMP/Cr ratio in human neoplasms of epithelial origin was often significantly lower than normal, irrespective of the extension of malignancy. Surgical resection of the tumour, radiotherapy, or theophylline treatment increased urinary excretion of the nucleotide. In patients with malignancy, intravenous infusion of glucagon failed to produce the degree of elevation of plasma cAMP seen in normal subjects. Urines from patients with malignant neoplasms had low values of cAMP/Cr ratio with increased values of cGMP/Cr ratio. These findings could be the result of systemic alteration in synthesis or breakdown of the nucleotides.
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PMID:Urinary excretion of cyclic adenosine 3',5'-monophosphate and cyclic guanosine 3',5'-monophosphate in malignancy. 21 Nov 47

To investigate the role of glucagon and insulin receptor binding in the glucagon hypersensitivity and insulin resistance which characterize the glucose intolerance of uremia, liver plasma membranes were prepared from control rats (blood urea nitrogen [BUN] 15+/-1 mg/100 ml, creatinine 0.7+/-0.2 mg/100 ml), and from 70% nephrectomized rats (BUN 30+/-2 mg/100 ml, creatinine 2.2+/-0.2 mg/100 ml), and from 90% nephrectomized rats (BUN 46+/-3 mg/100 ml, creatinine 4.20+/-0.7 mg/100 ml), 4 wk after surgery. As compared to controls, the 90% nephrectomized rats had significantly higher levels of plasma glucose (95+/-4 vs. 125+/-11 mg/100 ml), plasma insulin (28+/-9 vs. 52+/-11 muU/ml), and plasma glucagon (28+/-5 vs. 215+/-18 pg/ml). Similar, but less marked, elevations were observed in the 70% nephrectomized animals. In liver plasma membranes from nephrectomized rats, specific binding of (125)I-glucagon was increased by 80-120%. Furthermore, glucagon (2 muM)-stimulated adenylate cyclase activity in nephrectomized rats was twofold higher than in controls. In contrast, fluoridestimulated adenylate cyclase activity was similar in both groups of rats. In marked contrast to glucagon binding, specific binding of (125)I-insulin to liver membranes from nephrectomized rats was reduced by 40-50% as compared to controls. Data analysis suggested that the changes in both glucagon and insulin binding are a consequence of alterations in binding capacity rather than changes in affinity. Liver plasma membranes from nephrectomized rats degraded (125)I-glucagon and (125)I-insulin to the same extent as control rats. THESE RESULTS DEMONSTRATE THAT: (a) the 70 and 90% nephrectomized rats simulate the hyperglycemia, hyperinsulinemia, and hyperglucagonemia observed in clinical uremia; (b) in these animals specific binding of glucagon to liver membranes is increased and is accompanied by higher glucagon-stimulated adenylate cyclase activity; and (c) specific binding of insulin is markedly decreased. These findings thus provide evidence of oppositely directed, simultaneous changes in glucagon and insulin receptor binding in partially nephrectomized rats. Such changes may account for the hypersensitivity to glucagon and may contribute to resistance to insulin observed in the glucose intolerance of uremia.
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PMID:Glucagon and insulin binding to liver membranes in a partially nephrectomized uremic rat model. 700 82

Because the gastrointestinal hormones are known to dilate the splanchnic vasculature, their effects on transport of water and solutes during peritoneal dialysis were studied in an experimental model, the rabbit. In unanesthetized rabbits, dialysate volume was calculated by isotope dilution, and clearances were estimated by dialysate/plasma concentration ratio factored by minute volume. With isotonic dialysis solution, the mean increment in dialysate volume per minute of intraperitoneal dwell was 0.19 ml/kg/min, and mean clearances of creatinine and urea were 0.71 and 0.90 ml/kg/min, respectively. When administered intravenously, secretin significantly augmented osmotically induced water flux, but not when given intraperitoneally. Neither glucagon nor cholecystokinin affected dialysate volume. Intravenously, but not intraperitoneally, glucagon increased peritoneal clearances of creatinine and urea to more than 150% of control values. Neither cholecystokinin nor secretin augmented significantly peritoneal mass transport when given by either route. The data suggest that the site of acton is the endothelial surface of the membrane, that the mechanisms of augmenting transport involve increased permeability and/or surface area, and that agents which combine an increase in mass transport and capillary filtration coefficient may be clinically useful.
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PMID:Effects of gastrointestinal hormones on transport by peritoneal dialysis. 51 2

Fasting serum gastrin, cholecystokinin, glucagon, and gastric inhibitory polypeptide concentrations were simultaneously measured in normal subjects and in patients with different degrees of renal failure. Values of gastrin, cholecystokinin, gastric inhibitory polypeptide, and glucagon were significantly higher in all patients with serum creatinine concentrations greater than 3 mg/dl than in controls (P less than 0.01). The degree of renal insufficiency was significantly correlated (P less than 0.05) with serum concentrations of each hormone, but no significant linear correlation existed among the serum concentrations of different gastrointestinal hormones in individuals. Hemodialysis did not significantly alter predialysis serum gastrin, cholecystokinin, or glucagon concentration, but the serum gastric inhibitory polypeptide concentration decreased by 30% (P less than 0.01) after hemodialysis. The disproportionate increases of hormones with antagonistic actions may alter gastrointestinal function in renal insufficiency.
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PMID:Gastrointestinal hormone profile in renal insufficiency. 51 44

The peritoneal clearance of creatinine and inulin during isotonic peritoneal dialysis was studied in dogs before and after the administration of two vasodilators: isoproterenol and glucagon. One-liter exchanges with 15-min dwell times were used. Blood flow in the superior mesenteric artery was recorded with an electromagnetic flow probe and used as an index for total splanchnic flow. Intravenous isoproterenol (2.4 microgram/min) increased blood flow by 88%, but did not alter peritoneal clearance. When isoproterenol was given i.p. (0.5 microgram/ml dialysis fluid), blood flow increased by 81%, and inulin clearance rose by 26.8% (2.06 +/- 0.18 to 2.61 +/- 0.23 ml/min; P less than 0.05). Creatinine clearance increased by 17.5%, from 10.94 +/- 0.32 to 12.85 +/- 0.34 ml/min (P less than 0.05). When blood flow was returned to control levels with a clamp, clearances also returned to control levels. Glucagon given i.p. (1.0 microgram/ml) had no effect on any measured variable. Glucagon given i.v. at 10 microgram/min caused blood flow to rise by 81% and inulin clearance to rise by 25% from 1.88 +/- 0.16 to 2.35 +/- 0.19 ml/min (P less than 0.05). Cp, inulin clearance remained at control levels. Vasodilators seem to exercise two effects in augmenting clearance of small and middle-sized molecules: a direct permeability effect and a blood-flow related effect, possibly in increasing the surface area available for exchange and/or increasing permeability of the capillary endothelium.
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PMID:Peritoneal clearance of creatinine and inulin during dialysis in dogs: effect of splanchnic vasodilators. 54 92

The amylase/creatinine clearance ratio (Cam/Ccr ratio) was determined in 239 subjects. In 87 hospitalised patients without pancreatic disease (controls) the Cam/Ccr ratio was 3.02 +/- 0.69 (mean +/- ISD). The ratio was above the normal range in all patients with acute pancreatitis but was normal in those with chronic pancreatitis and carcinoma of the pancreas. In 18 patients with choledocholithiasis a raised ratio distinguished those with pancreatitis as assessed independently by the surgeon at laparotomy from those with a macroscopically normal pancreas. Raised Cam/Ccr ratios were also found in diabetics with ketoacidosis and in three patients with fulminant alcoholic liver disease. Though a positive correlation was found between the Cam/Ccr ratio and serum creatinine concentration, abnormally high ratios did not occur in 30 patients with chronic renal failure. A significant increase in Cam/Ccr ratios was produced in six healthy volunteers by intravenous injection of glucagon. However, it is unlikely that hyperglucagonaemia alone accounts for the increased Cam/Ccr ratio seen in acute pancreatitis, as no correlation was found between the clearance ratio and the plasma glucagon concentration in a series of patients. In two other patients in whom excess circulating pancreatic polypeptide was detected the Cam/Ccr ratio was normal. It is concluded that, in view of the sensitivity and relative specificity of finding an increased Cam/Ccr ratio in acute pancreatitis, its determination should be valuable clinically, especially in those cases of hyperamylasaemia where the cause is in doubt. The mechanism whereby the ratio is increased is unknown, and it is unlikely that either glucagon or pancreatic polypeptide is a major factor in its production.
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PMID:Mechanism and specificity of increased amylase/creatinine clearance ratio in pancreatitis. 60 90

Significant hypertriglyceridemia, the most common lipid abnormality in renal failure, first occurs when the creatinine clearance falls to 50 ml/min. The prevalence of hypertriglyceridemia continues to rise as creatinine clearance falls further with the highest rate developing at a creatinine clearance less than 10 ml/min. Hypertriglyceridemia is correlated with plasma glucagon levels but not growth hormone or insulin. Plasma cholesterol values remain normal in the face of deteriorating renal function and show no correlation with any of the hormones measured. Although all three hormones became elevated as renal function diminished, none were directly correlated with glomerular filtration rate. There was a distinct decrease in the prevalence of hyperlipidemia after 5 years of maintenance hemodialysis therapy. Plasma growth hormone and glucagon through an effect on plasma triglyceride and plasma insulin by effecting plasma cholesterol may play a role in this decline of hyperlipidemia with duration of hemodialysis.
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PMID:Relationship of plasma lipids to renal function and length of time on maintenance hemodialysis. 70 43

The investigations were carried out with a group of ten healthy men aged 20--26 years who were injected intravenously with glucagon in a single dose of 50 microgram per kg of body weight. Glucagon had no effect on myoinositol levels in the blood serum. It caused however, a significant decrease in the myoinositol discharge into urine and lowered the index of renal myoinositol clearance. The creatinine clearance index remained unchanged.
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PMID:The effect of glucagon on myoinositol levels in the blood serum and its excretion with urine. 74 10


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