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)

When compared to normal liver membranes, purified plasma membranes of regenerating liver and Morris hepatomas contain low but variable capacities to bind glucagon. This property is inversely related to the capacity of the isolated hepatocytes to bind to heterologous biomatrix glycoproteins. Since these parameters are characteristic of the proliferative state of the cells, it was important to further study the glucagon receptor protein and stimulation of adenylate cyclase activity. Our results show that 125I-iodinated plasma membranes obtained from normal liver contain three molecular species (117000, 98000, 86000 molecular weight) that can be eluted specifically with glucagon from a sepharose-glucagon affinity column. These proteins contain the putative glucagon receptor since binding of 125I- iodoglucagon is increased 150-fold as compared to unfractionated membranes. Plasma membranes obtained from Morris hepatoma (7800) and liver of chemically hepatectomized rats do not bind glucagon and lack these proteins. After inactivation with N-ethylmaleimide of the adenylate cyclase activity of the normal plasma membranes, they were fused with membrane of the hepatoma. The hybrid membranes showed 60% recovery of glucagon-stimulated cyclase activity. These results suggest that the plasma membranes of the proliferating liver cells do not contain receptor protein but have intact regulatory and catalytic subunits of the adenylate cyclase system.
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PMID:Lack of glucagon receptors in Morris hepatoma 7800. 632 89

Although its action at the molecular level is not completely understood, insulin, as well as its antagonist glucagon, certainly plays an important role in the modulation of protein synthesis. In order to observe whether insulin is involved in virus gene expression, we studied its effect on PLC/PRF/5 human hepatoma cell line, which posses HBV DNA sequences integrated at several sites. While human insulin had no effect on cell growth and increased the production of two plasma proteins, a selective inhibitory effect on HBsAg production could be detected. This observation might be useful for further studies both on virus gene expression and insulin action at the molecular level.
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PMID:Insulin reduces HBsAg production by PLC/PRF/5 human hepatoma cell line. Brief report. 633 47

Adenylate cyclase activity was measured in plasma membranes isolated from Morris Hepatoma 7800 and from control and host livers. The only difference found in tumor enzyme activity was the lack of response to glucagon. The membrane-binding capacities for the pancreatic hormones insulin and glucagon were measured. Hepatoma membranes did not bind glucagon. Insulin-binding parameters could not be determined because of high non-specific binding. The plasma levels of insulin in the tumor-bearing animals were approximately half of those found in controls, whereas the glucagon levels in plasma were 50% higher in tumor-bearing animals. Thyroxine and triiodothyronine plasma levels were reduced in tumor-bearing rats, while the thyroid-stimulating hormone level was within normal limits. The amount of cAMP (275 pmol g-1) and cGMP (3.6 pmol g-1) in the tumor were lower than in the host and control livers, but the ratio of cGMP to cAMP in the tumor was increased by a factor of 2. These results are discussed with respect to control mechanisms of cell proliferation in comparison with other hepato-proliferative states.
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PMID:Hormonal changes and adenylate cyclase system in rat bearing 7800 Morris hepatoma. 634 40

Hepatic stimulator substance (HSS), a partially purified extract of weanling or regenerating adult rat liver, is an organ-specific stimulator of liver growth in vivo and in vitro. The HTC hepatoma cell line is particularly responsive to HSS. The present experiments show that HSS will stimulate HTC cells in the complete absence of serum, although graded doses of fetal cal serum (FCS), from 0.1 to 5.0%, will increase the degree of stimulation in a dose-dependent manner. In contrast, when HSS is absent, increasing doses of FCS above 0.5% inhibit DNA synthesis. Much of this inhibition is removed by prior dialysis of the FCS and maximum enhancement of the HSS-induced stimulation occurs with only 0.1-0.5% of the dialysed FCS. Sera from older animals have less or even negative effect. Evidence is presented to show that the enhanced stimulation by HSS in the presence of serum is not due to insulin, glucagon, epidermal growth factor (EGF), or platelet derived growth factor (PDGF) and that HSS does not act via a shared receptor for one of these hormones. These experiments provide further evidence that HSS is a unique stimulator of liver growth and lend support to a model of organ-specific growth control.
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PMID:Stimulation of HTC hepatoma cell growth in vitro by hepatic stimulator substance (HSS). Interactions with serum, insulin, glucagon, epidermal growth factor and platelet derived growth factor. 636 7

When freshly-dispersed rat hepatocytes are maintained in primary monolayer cultures, they quickly lose their capacity to synthesize the urea cycle enzyme, carbamoyl-phosphate synthase. The ability to synthesize many other proteins, e.g., serum proteins including albumin, is retained. After an initial recovery period following cell isolation (24-48 h), glucagon is able to restore the ability of cultured hepatocytes to make carbamoyl-phosphate synthase. mRNA encoding the enzyme is about 4-times higher in hepatocytes maintained for 48 h in the presence of glucagon compared to hepatocytes without the hormone, as judged by in vitro translational assays. The level of carbamoyl-phosphate synthase activity expressed in transformed hepatocytes is unique to each hepatoma. Here we show that Morris hepatoma 5123D has retained such expression, and actively synthesizes the enzyme when 5123D cells are placed in monolayer cultures. Unlike normal hepatocytes, however, synthesis continues uninterrupted at a high level whether or not glucagon is present. 5123D has higher levels of translatable carbamoyl-phosphate synthase mRNA than normal liver.
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PMID:Effects of glucagon on biosynthesis of the mitochondrial enzyme, carbamoyl-phosphate synthase I, in primary hepatocytes and Morris hepatoma 5123D. 661 42

We find that the two wide-range Na+-dependent transport systems A and ASC for various neutral amino acid can be discriminated more sharply in the hepatoma cell line HTC than in any cell yet studied by us in which the two systems co-exist. The gain comes partly from a higher reproducibility and a higher relative ASC rate for HTC than in ordinary rat hepatocytes, also a repressed condition of System A unless first deprived of amino acids, but mainly from our finding that in the hepatoma cell threonine serves as a nearly specific substrate and inhibitor of System ASC, thus decisively supplementing older discriminatory techniques. In ordinary hepatocytes cysteine is quite specific to ASC as a substrate but not as an inhibitor, whereas threonine is specific in neither role. In the hepatoma cell cysteine in turn is specific in neither role. In addition to these and other differences between the two cells in analog specificity, which are partly assignable to System ASC and partly to System A, System ASC of the hepatoma cell shows an inhibition on lowering the pH from 6.5 to 5 not seen in the ordinary hepatocyte. Furthermore, threonine uptake by the hepatoma cell undergoes no stimulation when Li+ is substituted for choline in a Na+-free medium, whereas ASC uptake by the ordinary rat hepatocyte is stimulated much as is System A uptake. As in other occurrences, and in contrast to System A, ASC transport in the hepatoma cell is stimulated neither by amino acid deprivation nor by insulin, glucagon, or dexamethasone. Trans-stimulation, both inward and outward, via System ASC is vigorous in the hepatoma cell. Despite the surprising differences observed, common features of each system in various occurrences continue to justify the use of the abbreviations ASC and A as long as they are understood as generic designations.
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PMID:Surprising differences in substrate selectivity and other properties of systems A and ASC between rat hepatocytes and the hepatoma cell line HTC. 679 May 28

In tumor-bearing rats the hematocrit volume was decreased. It is recommended therefore to estimate the content of glucose in blood serum but not in the whole blood. In rats with Zajhdela ascites hepatoma and with solid hepatoma 27 contents of insulin and glucagon in blood and of glycogen in liver were altered. The nature and magnitude of these alterations varied depending on the type of the transplated tumor. The hormonal disbalance appears to be due to loss of receptor sensitivity towards these hormones. In blood serum of healthy and tumor-bearing rats maximal glucose content was observed within 30 min after sugar loading, after which the content of glucose in blood serum was decreased. In the tumor-bearing rats the increase in content of glucose after sugar loading was higher than in the healthy animals, and the return of content of glucose to normal values was considerably delayed in the tumor-bearing rats. Apparent Vass for glucose was distinctly lower in healthy as compared with tumor-bearing animals. Simultaneous increase in content of glucose and insulin was found in blood serum of healthy rats after sugar loading, whereas the increase in insulin content was retarded in the tumor-bearing animals.
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PMID:[Endocrine disorders caused by a tumor in the body]. 698 2

A patient with biopsy-proved biliary cirrhosis and previous gastrojejunostomy and portacaval anastomosis experienced episodes of severe hypoglycemia. She was found to have hyperinsulinemia and hyperglucagonemia. An oral glucose tolerance test showed postgastrectomy hypoglycemia. Results of the intravenous tolbutamide test were diagnostic for insulinoma, but results of the intravenous glucagon test and prolonged fast (96 hours) were not. Failure, on two occasions, to suppress C-peptide normally during insulin-induced hypoglycemia led to a diagnosis of pancreatogenous hyperinsulinemia. The pancreas showed a 10-fold increase in islet volume, with intensely positive staining with anti-insulin and anti-glucagon antiserums in addition to anti-somatostatin and anti-pancreatic polypeptide antiserums. Incidental findings at pancreatic exploration were a mesothelioma, which did not stain with anti-insulin antiserum, and, at autopsy one year later, a hepatoma.
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PMID:Diagnosis of pancreatic islet hyperplasia causing hypoglycemia in a patient with portacaval anastomosis. 699 72

Photoaffinity labeling techniques were used to identify insulin-binding components of the plasma membrane in insulin-responsive, monolayer-cultured hepatoma cells. The activated, photosensitive reagent, an n-hydroxysuccinimide ester of 4-azidobenzoic acid, was coupled with highly purified insulin, and the hormone derivative was subsequently iodinated, bound to cell surface receptors of intact H4 cells, and photoactivated. Ater dissolution of the cells, labeled proteins were analyzed by SDS/polyacrylamide gel electrophoresis under reducing conditions. The main labeled band exhibited an apparent molecular weight of 130,000. Two minor components of apparent mol wt 95,000 and 40,000 were also identified. Specific labeling of all 3 bands was inhibited by simultaneous incubation of the cells with native insulin, but not by the heterologous hormone, glucagon, prior to photoactivation. Binding of azidobenzoyl insulin to H4 cells was time-dependent, as was the correlated labeling of receptor components. Band-labeling by the photosensitive insulin derivative was totally light-dependent; spontaneous covalent linking of insulin and receptor was not observed. The labeled receptor-related proteins were not degraded by the cells under our experimental conditions.
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PMID:Photoaffinity labeling of the insulin receptor in H4 hepatoma cells: lack of cellular receptor processing. 701 74

1. Adenylate cyclase activity in homogenate and plasma membrane preparations from chicken liver and from Mc-29 virus induced transplantable hepatoma has been investigated. The basal enzyme activity from both liver and hepatoma homogenates and plasma membranes was similar. 2. NaF stimulated the enzyme activity in both liver and hepatoma plasma membranes, while only liver adenylate cyclase was activated by glucagon and epinephrine. 3. No inhibitory effect of insulin was established on liver and hepatoma enzyme activity. 4. Adenylate cyclase activity in liver and hepatoma plasma membranes was inhibited by colchicine at the same degree.
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PMID:Adenylate cyclase activity in plasma membranes of chicken liver and of Mc-29 virus induced hepatoma. 712 5


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