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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To elucidate the mechanism of glucagon-insulin (G-I) therapy, the effect of insulin and/or glucagon on the insulin receptor was studied in an experiment utilizing cultured cells (JTC-16) of rat ascites hepatoma. Insulin specific receptors were present on JTC-16 cells and were similar in nature to the receptors of primary culture rat hepatocytes. There were two kinds of insulin receptors. One had a high insulin affinity and the other had low insulin affinity. In the experiment involving addition of insulin the number of insulin receptors decreased after 24 hrs incubation in proportion to the increase in added insulin concentration. On the other hand, the number of insulin receptors increased with glucagon addition and the increase in proportion to the concentration of glucagon added. In the experiment involving simultaneous addition of insulin and glucagon, a 20% decrease in the number of receptors induced with 10(-9) M insulin was restored to the control level with simultaneous glucagon addition of the same concentration. The number of insulin receptors increased as the concentration of additive glucagon increased. These results show that simultaneous addition of insulin and glucagon inhibits the decrease in number of insulin receptors with insulin alone. These facts may obtain more potent action of insulin in G-I therapy via insulin receptor.
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PMID:The effect of insulin and glucagon on the insulin receptor of cultured hepatoma cells. 353 98

Glycogen phosphorylase a activity in 7 rat ascites hepatoma cell lines treated with adrenergic agents, phenylephrine, epinephrine and isoproterenol, was investigated as compared with that in freshly isolated rat hepatocytes. Basal phosphorylase activities in hepatoma cells except AH7974 cells were lower than that in hepatocytes. Phosphorylase in hepatoma cells was not activated by any of the agents, while the enzyme activity in hepatocytes was clearly increased in a dose- and time-dependent manner. Phosphorylase in hepatocytes was sensitive to glucagon, but it was found to be insensitive to glucagon in all hepatoma cells. The present results suggest that rat ascites hepatoma cells may escape the glycogenolytic regulation by catecholamines and glucagon.
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PMID:Studies on responsiveness of hepatoma cells to catecholamines. IV. Lack of adrenergic activation of phosphorylase in rat ascites hepatoma cells. 379 26

Insulin, glucagon, and epidermal growth factor (EGF) addition stimulated DNA synthesis in primary hepatocyte cell cultures prepared from adult rat liver. The addition of ethanol (20-200mM) to the culture medium resulted in a substantial reduction in DNA synthesis as measured by 3H-thymidine incorporation and autoradiography. This effect was specific for differentiated hepatocytes compared to fibroblasts and two other human hepatoma cell lines. These studies demonstrate in a cell culture system that one of the major properties of ethanol is the inhibition of hepatocyte DNA synthesis.
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PMID:Ethanol inhibits hormone stimulated hepatocyte DNA synthesis. 388 19

Treatment of rat hepatoma cells with insulin, glucagon, thyroxine (T4) and triiodothyronine (T3) caused a concentration-dependent decrease in the monomeric actin content as measured by the deoxyribonuclease-I inhibition assay. Similarly, human peripheral blood neutrophils responded with a decrease in monomeric actin content when stimulated with T4, T3 and the adrenergic agonists phenylephrine and isoprenaline. The effect of phenylephrine could be blocked by phentolamine, demonstrating the specificity of the interaction. These observations suggest that hormone-induced actin changes might be an important event in response to both cell-surface-reactive hormones, such as insulin, glucagon and adrenergic agents, and those hormones that act through intracellular receptors, such as thyroid hormones. It is suggested that changes in actin state may have a role in metabolic regulation and cell growth.
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PMID:Hormone-induced actin polymerization in rat hepatoma cells and human leucocytes. 390 27

HeLa S3 cells, a clonal strain adapted for growth in suspension culture, contain adenylate cyclase activity that is stimulated by glucagon, prostaglandin E(1), and epinephrine. Total enzymatic activity and response to hormones is increased as a result of these cells being in stationary culture for several days. The parental strain of HeLa cells normally grown in stationary culture shows even greater adenylate cyclase activity. Hepatoma (HTC) cells grown in suspension culture have no detectable adenylate cyclase activity, but when grown in stationary culture they contain low, but detectable, amounts of adenylate cyclase, which is stimulated by glucagon, epinephrine, or prostaglandins. Chang's liver cells, both suspension and stationary culture, contain relatively high levels of adenylate cyclase that is stimulated by epinephrine or prostaglandin E(1), with differences in activity depending upon culture conditions. Adenylate cyclase of 3T3 and L929 mouse fibroblasts respond to catecholamines, as well as to prostaglandin E(1), but not to glucagon. Characteristic increases in basal activity of adenylate cyclase and in activity in the presence of hormone occurred as cell density increased during stationary culture of certain cell lines, but do not occur with fluoride ion present. In addition to the influence of growth conditions and rate or phase of cell growth on cyclase activity and hormonal response, the cultured cell lines frequently showed marked differences in activity from one another; malignant cells generally exhibited less activity. It is postulated that adenylate cyclase activity may be enhanced by cell to surface contact or cell to cell interaction and that this phenomenon may represent a form of self regulation or modulation of hormonal response by a tissue.
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PMID:Conditions leading to enhanced response to glucagon, epinephrine, or prostaglandins by adenylate cyclase of normal and malignant cultured cells. 433 46

Alpha-aminoisobutyric acid transport in hepatoma cells in culture was increased by insulin but not by hydrocortisone. Both of these agents induce tyrosine aminotransferase activity in this system. The apparent increase in alpha-aminoisobutyric acid transport and tyrosine aminotransferase activity produced by glucagon is probably caused by insulin contamination. Insulin did not increase transport in this system until after tyrosine aminotransferase activity had reached maximum levels. The mechanisms underlying increased alpha-aminoisobutyric acid transport appear to differ from those for tyrosine aminotransferase induction with hydrocortisone despite their close association in previous whole animal experiments.
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PMID:Amino acid transport in hepatoma cell cultures during tyrosine aminotransferase induction. 439 27

Basic and stimulated intracellular cAMP concentrations were measured in normal chicken liver and MC-29-virus-derived transplantable hepatoma (VTH) slices after in vitro incubation. Data indicated the preservation of catecholamine receptor but a loss of glucagon receptor in VTH. Comparing the relative stimulatory action of various catecholamines on cAMP concentration it was concluded that as in normal liver a predominantly beta 2-adrenergic receptor exists in the VTH, but its response to adrenaline is greater. Vinca alkaloids induced higher cAMP concentration in VTH than in normal liver. This stimulation was abolished by glucagon, while catecholamines and Vincristine acted in a synergistic manner on cAMP concentration.
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PMID:Further studies on the biochemical characterization of the MC-29 virus derived transplantable hepatoma (VTH). II. Modification of cyclic adenosine-3',5'-monophosphate levels by catecholamines, glucagon and Vinca alkaloids in normal chicken liver and VTH. 609 66

Characteristic and patterns of gamma-glutamyltranspeptidase (GGT) expression were studied in four rat and three human hepatoma cell lines. Phenotypic diversity of GGT expression was demonstrated by the following findings. (a) GGT specific activity increased rapidly in three of four rat lines during the first 72 hr after subculture. (b) GGT activity was detected in the fourth rat cell line only from 96 to 120 hr after subculture. (c) In late log or stationary cultures, each of the four rat lines assumed a unique and characteristic level of GGT specific activity. (d) The intracellular GGT distribution pattern was markedly varied in rat and human cell lines. (e) GGT activity was confined to isolated cell clusters in one human line in vitro and one rat line both in vivo and in vitro. And (f) there was poor correlation between GGT specific activity and several liver-associated and hepatoma-associated properties. In contrast to evidence of diversity in GGT expression, GGT was shown to be a nonsecreted protein in all four rat cell lines. The constitutive or autogenous nature of the GGT phenotype in rat hepatoma cells was demonstrated by the retention of the GGT-positive and GGT-negative phenotypes of two strains grown in mixed culture; the lack of change in GGT activity when cells were cultured on different substrata, in different media, or in media containing hormones (insulin, dexamethasone, triiodothyronine, or glucagon); and the assumption of nearly constant levels of GGT specific activity in late log or stationary cultures. The results suggest that GGT activity is expressed in hepatomas as a result of disturbed differentiation and that this expression is not necessarily linked to cell proliferation.
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PMID:Phenotypic diversity of gamma-glutamyltranspeptidase activity and protein secretion in hepatoma cell lines. 612 Jul 61

Serum-free, hormonally defined media have been developed for optimal growth of a rat hepatoma cell line. The cells' hormonal requirements for growth are dramatically altered both qualitatively and quantitatively by whether they were plated onto tissue culture plastic or collagenous substrata. On collagenous substrata, the cells required insulin, glucagon, growth hormone, prolactin, and linoleic acid (bound to BSA), and zinc, copper, and selenium. For growth on tissue culture plastic, the cells required the above factors at higher concentrations plus several additional factors: transferrin, hydrocortisone, and triiodothyronine. To ascertain the relative influence of hormones versus substratum on the growth and differentiation of rat hepatoma cells, various parameters of growth and of liver-specific and housekeeping functions were compared in cells grown in serum-free, hormonally supplemented, or serum-supplemented medium and on either tissue culture plastic or type I collagen gels. The substratum was found to be the primary determinant of attachment and survival of the cells. Even in serum-free media, the cells showed attachment and survival efficiencies of 40-50% at low seeding densities and even higher efficiencies at high seeding densities when the cells were plated onto collagenous substrata. However, optimal attachment and survival efficiencies of the cells on collagenous substrata still required either serum or hormonal supplements. On tissue culture plastic, there was no survival of the cells at any seeding density without either serum or hormonal supplements added to the medium. A defined medium designed for cells plated on tissue culture plastic, containing increased levels of hormones plus additional factors over those in the defined medium designed for cells on collagenous substrata, was found to permit attachment and survival of the cells plated into serum-free medium and onto tissue culture plastic. Growth of the cells was influenced by both substrata and hormones. When plated onto collagen gel substrata as compared with tissue culture plastic, the cells required fewer hormones and growth factors in the serum-free, hormone-supplemented media to achieve optimal growth rates. Growth rates of the cells at low and high seeding densities were equivalent in the hormonally and serum-supplemented media as long as comparisons were made on the same substratum and the hormonally supplemented medium used was the one designed for that substratum. For a given medium, either serum or hormonally supplemented, the saturation densities were highest for tissue culture plastic as compared with collagen gels.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Regulation of growth and differentiation of a rat hepatoma cell line by the synergistic interactions of hormones and collagenous substrata. 613 87

Of all available liver cells in culture, only primary cultured hepatocytes are known to respond to glucagon in vitro. In the present study we investigated whether glucagon could stimulate amino acid transport and tyrosine aminotransferase (TAT;EC 2.6.1.5) activity (two well-characterized glucagon effects in the liver) in Fao cells, a highly differentiated rat hepatoma cell line. We found that glucagon had no effect on transport of alpha-aminoisobutyric acid (AIB; a non-metabolizable alanine analogue) nor on TAT activity, even though both activities could be fully induced by insulin [2-fold and 3-fold effects for AIB transport and TAT activity, respectively, after 6h; EC50 (median effective concentration) = 0.3 nM], or by dexamethasone (5-8-fold effects after 20 h; EC50 = 2 nM). Analysis of [125I]iodoglucagon binding revealed that Fao cells bind less than 1% as much glucagon as do hepatocytes, whereas insulin binding in Fao cells was 50% higher than in hepatocytes. The addition of dibutyryl cyclic AMP, which fully mimics the glucagon stimulation of both AIB transport and TAT activity in hepatocytes, induced TAT activity in Fao cells (a 2-fold effect at 0.1 mM-dibutyryl cyclic AMP) but had no effect on AIB transport. Cholera toxin stimulated TAT activity to the same extent as did dibutyryl cyclic AMP. These results indicate that the lack of glucagon responsiveness in cultured hepatoma cells results from both a receptor defect and, for amino acid transport, an additional post-receptor defect. Moreover, the results show that amino acid transport and TAT activity, which appeared to be co-induced by insulin or by dexamethasone in these cells, respond differently to cyclic AMP. This suggests that different mechanisms are involved in the induction of these activities by glucagon in liver.
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PMID:Glucagon resistance of hepatoma cells. Evidence for receptor and post-receptor defects. 613 31


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