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)

Two groups of Sprague-Dawley rats, Harlan (H) and Charles River (CR), were discovered in that the medullary thick ascending limb (MAL) had a profoundly different adenylate cyclase response to arginine vasopressin (AVP). Using these two groups of rats, we studied the correlation between AVP action on the MAL and maximal urinary concentration. AVP (10(-6) M) significantly stimulated adenylate cyclase in MAL of H rats (7.4 +/- 0.9 to 43.8 +/- 4.6 fmol cAMP formed X 30 min-1 X mm-1, P less than 0.001) but not in CR rats (10.3 +/- 1.4 to 12.7 +/- 2.0 fmol cAMP formed X 30 min-1 X mm-1, NS). In contrast, AVP significantly stimulated adenylate cyclase of cortical, outer and inner medullary collecting tubules from both H and CR rats. Glucagon (10(-6) M) significantly stimulated adenylate cyclase of MAL from both H and CR rats. After 48 h of fluid deprivation, urinary osmolality was significantly higher (P less than 0.001) in the H (4,504 +/- 399 mosmol/kg H2O, n = 14) than CR (2,840 +/- 176 mosmol/kg H2O, n = rats. This observation was not attributable to differences in creatinine clearance (CR, 1.30 +/- 0.24; H, 1.24 +/- 0.03 ml/min, NS, n = 4) or plasma AVP (CR, 12.75 +/- 1.44; H, 12.38 +/- 1.17 pg/ml, NS, n = 6) levels. These results therefore suggest that the action of AVP on the MAL, in addition to the effect on collecting tubules, is involved in maximal urinary concentration in rats.
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PMID:Role of arginine vasopressin in medullary thick ascending limb on maximal urinary concentration. 374 Feb 73

Glomerular filtration rate (GFR) by clearance of inulin and creatinine and effective renal plasma flow (ERPF) by para-aminohippurate clearance was investigated in 8 normal volunteers on low protein (LP) and high protein (HP) diet for 6 days in the basal state and after a mixed protein-rich test meal. Plasma immunoreactive insulin (IRI), glucagon (IRG) and growth hormone (IRHGH) were followed before and after the test meal. GFR was higher on HP than on LP diet and increased within one hour after the test meal. ERPF also increased significantly after the meal on LP diet. IRI increased maximally at 60 min after the test meal and then declined gradually. IRG increased after a latency period of 90 min and IRHGH consistently did not change. Since the increase in GFR was significant already one hour after the test meal, i.e. before IRG was changed, we conclude that glucagon is not a mediator of the protein-induced increased in GFR. Neither insulin nor growth hormone appeared to be involved.
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PMID:Influence of protein intake on renal hemodynamics and plasma hormone concentrations in normal subjects. 388 48

The effects of parathyroid hormone (PTH) on plasma and urinary adenosine 3',5'-monophosphate (cyclic AMP) levels were studied in normal subjects. Under basal conditions normal adults have plasma concentrations of cyclic AMP ranging from 10 to 25 nmoles/liter and excrete from 1.5 to 5 mumoles of cyclic AMP per g of urinary creatinine. About one-half to two-thirds of the cyclic AMP excreted in the urine is derived from the plasma by glomerular filtration, and the remainder is produced by the kidney. Renal production of cyclic AMP is partly under the control of PTH. It can be suppressed by infusions of calcium and stimulated by infusions of the calcium chelating agent, EDTA. Infusions of PTH in doses up to 10 mU/kg per min were associated with dose-related increases both in urinary cyclic AMP and phosphate. Infusions of PTH in doses ranging from 20 to 80 mU/kg per min did not lead to any further increase in phosphaturia but did lead to further marked increases in urinary cyclic AMP. A modest increase in plasma cyclic AMP was noted when PTH was infused at 40 mU/kg per min. Anephric patients failed to show appreciable increases in plasma cyclic AMP in response to large doses of PTH but did show expected increases in response to glucagon. Surgical removal of parathyroid adenomas from nine patients with primary hyperparathyroidism was invariably followed by a decrease in urinary cyclic AMP, PTH, in large doses, and calcium infusion produced up to 2-fold increases in the other known naturally occurring cyclic nucleotide, guanosine 3',5'-monophosphate (cyclic GMP).
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PMID:Effects of parathyroid hormone on plasma and urinary adenosine 3',5'-monophosphate in man. 548 Aug 62

Hyperglucagonemia accompanies several clinical conditions characterized by increased amylase/creatinine clearance. We tested the hypothesis that glucagon may be responsible for this augmented clearance. Therefore, a constant glucagon infusion was given to eight volunteers in order to attain physiological levels comparable to those obtained during acute pancreatitis. The amylase/creatinine clearance increased from 0.84 +/- 0.8% to a mean of 1.30 +/- 1.14% (p less than 0.001). This was, however, less than the clearance of 2.94 +/- 0.23% observed during acute pancreatitis. The rise in amylase clearance during acute pancreatitis is, therefore, only partially explained by the hyperglucagonemia.
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PMID:Hyperglucagonemia--a partial explanation for the increased amylase/creatinine clearance in pancreatitis. 618 41

Glucagon effects on the kidney include increased water, creatinine, and amylase clearance. We have compared these effects in several laboratory animal species. Although every species responded to glucagon, 1 mg iv, by some alteration in renal function there were differences in the degree and direction of the changes. Glucagon caused an increase in amylase clearance in four of the six species studied and an increase in creatinine clearance in four. An increase in urine flow tended to occur in all species. An increased amylase clearance is a feature of acute pancreatitis, and raised glucagon levels have been found during attacks. It is possible that the two are causally related. In the experimental situation, timing of urine collections and species differences were found to be of critical importance in exploring this possibility.
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PMID:The effect of glucagon on urine amylase in various animal species. 619 80

Increase in amylase excretion in the urine in response to 8 days of aerobic running is delayed until after the athletes have rested for 24-48 h. In contrast, the amylase creatinine ratio is increased immediately after intense short-term exercise. The mechanism for these differences is unknown, but the timing of the amylase excretion pattern after long- and short-term exercise is similar to the urinary amylase after continuous and single bolus intravenous glucagon.
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PMID:Amylase excretion after exercise. 620 84

The concentration of cyclic AMP which is known as an intracellular mediator of hormone action increased in the plasma of patients with chronic renal failure (CRF). In the present study, the plasma concentration of cyclic AMP significantly correlated not only with serum, creatinine, and urea levels, but also with plasma PTH and glucagon in patients with CRF. Furthermore, plasma concentrations of PTH and glucagon correlated with the serum creatinine concentration to a significant extent. To discuss the cause of the increased cyclic AMP concentration in plasma of patients with CRF, multivariate analyses were carried out on the obtained clinical data from patients and normal subjects. In the factor analysis on the clinical data from 61 subjects, cyclic AMP, creatinine and BUN correlated with the first factor and PTH correlated with the second factor. The cumulative contribution ratio by the second factor was 76%. The results of the cluster analysis indicated that cyclic AMP, creatinine, and BUN formed a cluster and PTH glucagon made another cluster. These results suggest that the elevated plasma concentration of cyclic AMP in patients with CRF was mainly introduced not by overproduction but by the retention of cyclic AMP due to the decreased renal function.
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PMID:A multivariate factor analysis of the high plasma concentration of cyclic AMP in patients with chronic renal failure. 624 11

Binding sites for human GH (hGH) were studied in liver membranes of rats with chronic renal insufficiency (CRI) associated with marked growth retardation. A subtotal nephrectomy was performed in young female rats. One month after the nephrectomy, the animals with a plasma creatinine level 3 times or more that of controls were studied; their mean statural gain was 56% that of controls. The specific binding of [125I]hGH to microsomal membranes of rats with CRI was low (40% that of controls). The number of binding sites rather than the affinity of the binding was affected; both the lactogenic and somatotropic sites were decreased, as judged from the binding of ovine [125I]PRL and bovine [125I]GH. The binding sites of the plasma membranes as well as those of the Golgi fractions, were reduced. In plasma membranes of rats with CRI, the specific binding of glucagon was low, and the specific binding of insulin was elevated; these modifications were associated with a high plasma glucagon level and a decreased insulinemia in rats with CRI, but no modification of plasma GH and PRL levels was found. Thus, the hormone level does not appear to regulate the GH-binding sites in this system. The link between the growth defect and the decreased number of GH-binding sites in the liver membranes of rats with CRI remains to be established.
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PMID:Lactogenic and somatotropic binding sites in liver membranes of rats with renal insufficiency. 624 58

Urinary c-AMP and c-GMP levels were measured in male and female F344/DuCrj rats during dietary treatment with 2% sodium o-phenylphenate (OPP-Na) for 136 days. At the end of the experiment, levels of the cyclic nucleotides in the plasma, kidney and liver, and of adenylate cyclase in the kidney and liver were also determined. Urinary c-AMP/creatinine in males decreased immediately after the start of OPP-Na treatment and recovered to the normal level within 1 wk. Such a biphasic change recurred intermittently until the end of the experiment. In the case of treated females, urinary c-AMP/creatinine also showed a decrease and recovery in 1 wk but no subsequent decrease was observed. As urinary c-GMP/creatinine in treated males was higher than that in control males, low c-AMP/c-GMP ratios persisted throughout the experiment. Although there was no significant difference of c-AMP or c-GMP levels in the liver or kidney between control and treated animals, c-AMP/c-GMP ratios in these tissues from treated rats decreased slightly. The c-AMP levels in plasma from treated males were significantly lower than those in the male controls, but no significant difference was observed between treated and control females. In the presence of activators (sodium fluoride, glucagon, epinephrine), adenylate cyclase activity in liver and kidney homogenates from treated rats was only about 70% of the control activity, except with the female kidney enzyme. This observed inhibition in treated rats suggests that the decreased excretion of urinary c-AMP in treated rats was not due to a decrease in renal clearance but to reduced production of c-AMP.
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PMID:Altered levels of cyclic nucleotides in F344 rats fed sodium o-phenylphenate. 632 89

Since glucagon and insulin (G/I) have been suggested to be hepatotrophic substances, the effect of G/I infusion on the ability to excrete water and sodium was tested in seven patients with cirrhosis and ascites (decompensated group), and compared with that in seven cirrhotics without ascites (compensated group). A constant infusion of 1 U glucagon and 10 U regular insulin over 2 hours daily for 14 days resulted in a significant improvement of prothrombin time in the decompensated group. Concomitantly, an increase in urine volume (62%, p less than 0.02) and a tendency toward an increase in urinary sodium excretion (68%, 0.05 less than p less than 0.1) were observed only in the decompensated group after the G/I infusion. In addition, these were associated with increases in creatinine clearance and osmotic clearance. These results suggest that glucagon and insulin merit further study in hepatorenal syndrome cases.
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PMID:Effect of simultaneous administration of glucagon and insulin on renal function in patients with liver cirrhosis and ascites. 637 77


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