Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Insulin causes a 7-10-fold decrease of both the mRNA that codes for rat hepatic phosphoenolpyruvate carboxykinase (mRNAPEPCK) and of PEPCK synthesis, provided the animals are made diabetic and fed chow. mRNAPEPCK, measured either by in vitro translation or cDNA hybridization, decreases with a half-time of 30-60 min after insulin treatment. This coordinant decrease, which approximates the half-life of mRNAPEPCK measured in a variety of situations, suggests that insulin acts by decreasing mRNAPEPCK production, and that the hormone does not alter the activity of a fixed amount of this RNA, or enhance its degradation. Glucagon results in a ninefold induction of mRNAPEPCK. Half-maximal induction occurs with doses between 20-75 micrograms/100 g body wt and occurs within 30-45 min. Maximal induction requires 150 micrograms/100 g body wt and occurs about 80 min after a single glucagon injection. N6,O2'-dibutyryl cAMP and a cAMP analogue that is not metabolized, 8-(4-chlorophenyl-thio)cAMP, induce mRNAPEPCK as effectively as glucagon and with similar kinetics. Since sodium butyrate, adenosine, and dibutyryl cGMP are ineffective inducers, cAMP appears to be the active agent in the hepatocyte.
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PMID:Insulin and glucagon regulate cytosolic phosphoenolpyruvate carboxykinase (GTP) mRNA in rat liver. 632 36

A system for isolation of capillaries from the retina has been adapted to biochemical studies in vitro. Insulin receptors were identified in human and calf retinal blood vessels. Binding of 125I insulin by calf retinal blood vessels takes place through high affinity (low capacity) and low affinity (high capacity) receptor sites. Insulin binding is inhibited by glucagon, and cGMP and proinsulin. Dissociation of insulin receptor protein or lipid with Triton X-100 or phospholipase results in significant decreases in 125I insulin binding by retinal blood vessels. Dissociation of insulin bound occurs only at 0 degrees C which may be due to rapid internalization of insulin at higher temperatures. Activities of cAMP and cGMP phosphodiesterases and cyclase of retinal vessels were not significantly changed by incubation with insulin. At high concentrations in the media human growth hormone stimulates and then inhibits I125 insulin binding by retinal capillaries.
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PMID:Insulin receptors in calf and human retinal blood vessels. 634 40

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

Exposure of isolated hepatocytes to glucagon for 45 min caused a 2.5-fold increase in the time (Ca2+ retention time) for which mitochondria subsequently isolated from the cells retained a load of exogenous Ca2+ before its spontaneous release. Half maximal effect of glucagon was observed at a concentration of 0.6 nM. An increase in the Ca2+ retention time was observed after 30 but not 15 min exposure of cells to the hormone. Incubation of hepatocytes with dexamethasone, epinephrine, vasopressin, dibutyryl cyclic AMP or 8-bromo cyclic GMP also induced an increase in mitochondrial Ca2+ retention time. The effect of glucagon was associated with an increase in cellular cyclic AMP and was inhibited by puromycin, cycloheximide and cordycepin, but not by actinomycin D or chloramphenicol. Puromycin caused only a small inhibition of the stimulation by glucagon of mitochondrial pyruvate carboxylation. It is concluded that the effects of glucagon on mitochondrial Ca2+ retention require nuclear DNA-directed protein synthesis and differ, in this respect, from the rapid-onset effects of the hormone on other mitochondrial properties, including pyruvate carboxylation.
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PMID:On the effect of glucagon on mitochondrial calcium retention in isolated hepatocytes. 650 Apr 86

The generation of T-cell colonies from human peripheral blood lymphocytes is a sensitive in vitro measure of cell-mediated immunity, considered to be under different and/or additional regulatory controls than short-term liquid cultures. The influences of steroids (aldosterone, estradiol, diethylstilbestrol, hydrocortisone, prednisolone, progesterone, testosterone), prostaglandins (PGA1, PGA2, PGB1, PGB2, PGE1, PGE2, PGF1 alpha), bradykinin, cyclic adenosine monophosphate (AMP), cyclic guanosine monophosphate (GMP), epinephrine, glucagon, histamine, insulin, luteinizing hormone, luteotropic hormone, serotonin, and thyroxin on the generation of both T-cell colonies in semisolid phase and induction of transformation in liquid culture was assessed in parallel assays. Steroids uniformly suppressed both types of culture systems, although colony formation appeared more sensitive by several hours of magnitude. In contrast, significant differences in the response of lymphocytes in colony formation assay, compared to liquid transformation, was noted for the other agents. Prostaglandins significantly inhibited colony formation even in the presence of as little as 10(-12) M PGE2; however, liquid culture responses were suppressed only by higher concentrations (10(-5) M) and enhanced transformation was found at lower concentrations (10(-9) M). Bradykinin, glucagon, and luteinizing hormone did not significantly influence either colony formation or liquid transformation. In contrast, cyclic AMP inhibited and cyclic GMP stimulated colony formation and liquid transformation. Histamine, insulin, epinephrine, and serotonin all had significant positive or negative influences on colony formation in concentrations that produced no detectable effects using conventional liquid transformation assays. Finally, correlation analysis of drug effects for each system extends the thesis that these assays quantitate different parameters of T-cell function. T-lymphocyte colony formation is a promising diagnostic tool for rapid screening of immune modulating agents.
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PMID:Pharmacologic and biochemical modulation of human T-lymphocyte colony formation: hormonal influences. 697 65

Gastric HCO3(-) transport (basal) studied in isolated amphibian mucosa and mammalian stomach in vivo amounts to 2-10% of maximal H+ secretion. Duodenal mucosa, devoid of Brunner's glands, transports HCO3(-) at a greater rate (per unit surface area) than either stomach or jejunum in vitro and in vivo. Gastric (but not duodenal) HCO3(-) transport is stimulated by dibutyryl cGMP, carbachol, and cholecystokinin and duodenal (but not gastric) transport by dibutyryl cAMP and gastric inhibitory peptide. Glucagon and E- and F-type prostaglandins stimulate, whereas histamine, gastrin, and secretin are without effect in both stomach and duodenum. Gastric transport very probably occurs by Cl--HCO3(-) exchange at the luminal membranes of the surface epithelial cells. In addition to this mechanism, the duodenum also transports HCO3(-) electrogenically. Lowering the luminal pH increases transport in both the stomach and duodenum. This response, probably mediated via both local production of prostaglandins and tissue-specific humoral agents, may be important in mucosal protection against acid. Metabolism-dependent transport of HCO3(-), stimulated by acid, seems quantitatively sufficient to account for all of the duodenal and most of the gastric mucosa's ability to remove luminal acid.
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PMID:Gastroduodenal HCO3(-) transport: characteristics and proposed role in acidity regulation and mucosal protection. 703 51

In primary cultured monolayer hepatocytes of adult rats, insulin (1 x 10(-8) M) induced glucose-6-phosphate dehydrogenase [EC 1.1.1.49, G6PDH] several fold in 48 h. It also induced lipogenesis, measured as [1-14C]acetate incorporation in 2 h, in these cells. Of the various lipids, triglycerides and phospholipids were induced markedly, while cholesterol and its esters were not induced. The increase of G6PDH and lipogenesis were parallel. Glucagon, dibutyryl cyclic AMP, triiodothyronine, dexamethasone, epinephrine, isoproterenol, and dibutyryl cyclic GMP were also tested under similar conditions, but none of them caused significant induction of G6PDH or lipogenesis. Use of anti-G6PDH serum showed that induction of G6PDH by insulin was due to increase in the amount of enzyme protein. Insulin was found to increase the rate of synthesis of G6PDH about 3-fold. SDS-polyacrylamide gel electrophoresis of the immunoprecipitable protein revealed that besides G6PDH another radioactive fraction (Mr 37,000) was increased by insulin. This suggests that complete synthesis of G6PDH protein is slowed down in primary cultured hepatocytes and that an apparent nascent peptide of the enzyme accumulates. Although on long-term treatment (48 h), glucagon and dibutyryl cyclic AMP had no effect on lipogenesis, when added with [14C]acetate for 2 h they strongly inhibited lipogenesis. Significant inhibition of lipogenesis by short-term treatment with glucagon was seen even in cells with a high capacity for lipogenesis induced by long-term treatment with insulin. Insulin again stimulated lipogenesis in short-term treatment, but its effect was slight. It is concluded from these results that insulin exerts long-term stimulation of lipogenesis by inducing enzymes related to lipogenesis including G6PDH as well as causing slight stimulation by enhancing supply of substrate for lipogenesis. Glucagon seems to play a minor role in long-term control, but it causes short-term inhibition of lipogenesis.
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PMID:Hormonal regulations of glucose-6-phosphate dehydrogenase and lipogenesis in primary cultures of rat hepatocytes. 704 Mar 64

The effects of trifluoperazine on the activation of glycogenolysis by various hormones were studied in perfused rat liver. Trifluoperazine significantly inhibited glycogenolytic effect of phenylephrine and angiotensin II by lowering maximal response, and that of vasopressin by shifting the dose-response curve to the right, while alpha-antagonist phentolamine was inhibitory only to phenylephrine. Phosphorylase activation of phenylephrine was inhibited by trifluoperazine in parallel with glycogenolytic response. The increase in 45Ca2+ efflux induced by phenylephrine, angiotensin II, and vasopressin was also inhibited by the agent. These inhibitory effects of trifluoperazine were not related to the change in tissue cyclic AMP or cyclic GMP levels. On the other hand, neither the glycogenolytic effect of glucagon, cyclic AMP, and N6,O2-dibutyryl cyclic AMP nor phosphorylase activation by glucagon was affected by trifluoperazine. Thus, trifluoperazine specifically inhibits the activation of glycogenolysis by Ca2+-dependent hormones.
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PMID:Inhibition by trifluoperazine of glycogenolytic effects of phenylephrine, vasopressin, and angiotensin II. 717 14

The hormonal responsiveness profile of the cortical collecting duct varies from one species to another. To identify the hormones and agonists that modulate the functions of this tubule segment in the human species, we generated a cell line (HCD) immortalized by SV40 virus. The tubular origin of this cell line was assessed by the expression of collecting duct-specific antigens and the ability of vasopressin to increase by nine-fold cAMP synthesis. Glucagon and adenosine stimulated cAMP synthesis, and atrial natriuretic peptide stimulated cGMP synthesis in a concentration-dependent manner. Bradykinin, adenosine and angiotensin increased intracellular calcium concentration ([Ca2+]i). Because adenosine can regulate tubular functions, we examined its role on glucagon-induced cAMP synthesis. Using adenosine analogs, we demonstrated that HCT cells both expressed adenosine type-2 (A2) receptors which stimulated cAMP production, and adenosine type-1 (A1) receptors linked to [Ca2+]i increase which inhibited glucagon-stimulated cAMP synthesis. The inhibitory effect was abolished by pertussis toxin, and was neither due to [Ca2+]i increase nor to protein kinase C activation, which indicated that some A1 adenosine receptors were directly negatively coupled to adenylyl cyclase. These results suggest that adenosine can modify human cortical collecting duct functions in opposite ways according to the adenosine receptor activated.
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PMID:Role of adenosine on glucagon-induced cAMP in a human cortical collecting duct cell line. 763 60

Hormonal and non-hormonal regulation of glucokinase gene expression was investigsted in cultured rat islet cells. To measure glucokinase mRNA in pancreatic islet cells, the competitive PCR method was adopted. With this method, GKmRNA levels can be measured using only 0.1-1.0 microgram of total RNA isolated from cultured rat islet cells. Following 24 h preculture with 5.5 mM glucose, islet cells were cultured for 24 or 8 h with hormonal or non-hormonal factors. Glucokinase mRNA levels tended to increase, but not significantly, at 16.7 mM glucose compared to those at 5.5 mM glucose. Treatment with either 1 microM T3 or 1 microM glucagon resulted in a decrease in the glucokinase mRNA level with 16.7 mM glucose, whereas 1 microM insulin had no effect on glucokinase mRNA. Five mM dibutyryl cyclic AMP decreased the glucokinase mRNA level with 16.7 mM glucose, but cycloheximide did not block this inhibitory effect, suggesting that the effect of glucagon may be mediated by cyclic AMP and that protein synthesis is not involved in the response. Furthermore, the islet glucokinase mRNA level increased in response to 1 microM glibenclamide with 5.5 mM glucose and the response was abolished by cycloheximide, which indicates the involvement of protein synthesis in the glibenclamide-induced mRNA change. An 8-bromo-cyclic GMP (1 microM) and vanadate (1 microM) did not affect the islet GKmRNA level. These findings suggested that thyroid hormone and glucagon-cyclic AMP suppress, and glibenclamide increases the GKmRNA level in cultured rat islet cells, and that insulin, cyclic GMP and vanadate differentially affect glucokinase gene expression in pancreatic islet cells and in the liver.
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PMID:Regulation of glucokinase gene expression in cultured rat islet cells: the inhibitory effects of T3 and glucagon, and the stimulatory effect of glibenclamide. 766 33


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