Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mongrel dogs were prepared by cholecystectomy, ligation of the lesser pancreatic duct, and insertion of modified Thomas cannulas into the duodenum and stomach. After recovery from surgery, experiments were performed by cannulation of the common bile duct for bile collection through the duodenal cannula. Bile flow and composition and the biliary clearance of erythritol were observed during secretin, glucagon, or sodium taurocholate choleresis and were compared with control studies. All test substances caused increased bile secretion. Sodium taurocholate caused a marked increase in bile salt output and in the biliary clearance of erythritol. Secretin caused a large increase in bile flow, no increase in bile salt output, and a very small increase in the biliary clearance of erythritol. The results indicate marked differences in the choleretic mechanism of sodium taurocholate and secretin and suggest that the principal action of taurocholate was on the canaliculi and the principal action of secretin was on the ducts.
 ...
PMID:The choleretic mechanisms of sodium taurocholate, secretin, and glucagon. 114 27

We have utilized canalicular (cLPM) and basolateral (blLPM) liver plasma membrane vesicles to investigate the domain localization of several Na(+)-dependent amino acid transporters. Neutral amino acid transport by systems N and ASC was measurable in both domains but was greater in blLPM vesicles. Sodium-dependent glutamate uptake (system X-) was preferentially localized to cLPM. The absolute activity and domain distribution of these three carriers remained unchanged after treatment of rats with a combination of glucagon and dexamethasone. A low level of basal system A activity was present in both the blLPM and cLPM. Glucagon-induced system A activity was first observed in blLPM vesicles approximately 60 min posthormone treatment and, in cLPM vesicles, approximately 30 min later. In situ perfusion of glucagon-treated rat liver with the membrane-impermeant protein modification reagent glutathione maleimide specifically inactivated blLPM system A activity and abolished the delayed arrival of hormone-induced activity to the cLPM. Transient perfusion of the liver with glutathione maleimide followed by a recovery period in vivo showed that the reagent did not irreversibly inactivate the transcytotic process and also provided an independent demonstration of the time delay between arrival of the carrier activity at the two membrane surfaces. These results support the concept of a transcytotic process in which the blLPM is the sorting site for the hormone-induced system A carrier proteins that eventually reach the cLPM.
 ...
PMID:Plasma membrane domain localization and transcytosis of the glucagon-induced hepatic system A carrier. 133 91

We report further characterisation of the hepatocyte growth factor 'hepatotropin' which is found in rat serum 24 h after partial hepatectomy. Hepatotropin enhances DNA synthesis in primary cultures of adult rat hepatocytes, and is of high molecular weight. Serum fractions were separated by gel filtration, heparin-sepharose affinity chromatography and ion-exchange chromatography. Sodium dodecylsulphate-polyacrylamide gel electrophoresis (SDS-PAGE) identified a band of apparent subunit relative molecular weight (Mr) 100,000 associated with biological activity, although purification to homogeneity has not been achieved. The activity is heat-labile, trypsin-sensitive, and stable to lyophilisation, but loses activity after dilution and reconcentration. In combination with known peptide hepatocyte growth modulators, hepatotropin acted synergistically with insulin and epidermal growth factor (EGF) but its action was not enhanced by glucagon. Studies on isolated rat hepatocyte membranes showed no evidence of enhanced phosphorylation of the EGF receptor by hepatotropin. The relationship of hepatotropin to previously described serum and platelet-derived growth factors is discussed.
 ...
PMID:Further characterisation of 'hepatotropin', a high molecular weight hepatotrophic factor in rat serum. 268 95

Various effectors, which act upon ion gradients, protein synthesis, membrane components or cellular functional groups, have been employed to provide insights into the nature of amino acid-membrane transport processes in animal cells. Such effectors, for example, include ions, hormones, metabolites and various organic reagents and their judicious use has allowed the following list of conclusions. Sodium ion has been found to stimulate amino acid transport in a wide variety of cell systems, although depending on the tissue and/or substrate, this ion may have no effect on such transport, or even inhibit it. Amino acid transport can be stimulated in some cell systems by other ions such as K+, Li+, H+ or Cl-. Both H+ and K+ have been found to be inhibitory in other systems. Amino acid transport is dependent in many cell systems upon an inwardly directed Na+ gradient and is stimulated by a membrane potential (negative cell interior). In some cell systems an inwardly directed Cl- and H+ gradient or an outwardly directed K+ gradient can energize transport. Structurally dissimilar effectors such as ouabain, Clostridium enterotoxin, aspirin and amiloride inhibit amino acid transport presumably through dissipation of the Na+ gradient. Inhibition by certain sugars or metabolic intermediates of the tricarboxylic acid cycle may compete with the substrate for the energy of the Na+ gradient or interact with the substrate at the carrier level either allosterically or at a common site. Stimulation of transport by other sugars or intermediates may result from their catabolism to furnish energy for transport. Insulin and glucagon stimulate transport of amino acids in a variety of cell systems by a mechanism which involves protein synthesis. Microtubules may be involved in the regulation of transport by insulin or glucagon. Some reports also suggest that insulin has a direct effect on membranes. In addition, a number of growth hormones and factors have stimulatory effects on amino acid transport which are also mediated by protein synthesis. Steroid hormones have been noted to enhance or diminish transport of amino acids depending on the nature of the hormone. These agents appear to function at the level of protein synthesis. While stimulation may involve increased carrier synthesis, inhibition probably involves synthesis of a labile protein which either decreases the rate of synthesis or increases the rate of degradation of a component of the transport system.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Effectors of amino acid transport processes in animal cell membranes. 286 64

1. The renal actions of ANP (average dose 30 ng kg-1 min-1 and glucagon (50 ng kg-1 min-1) were compared using fractional lithium reabsorption as the index of proximal reabsorption in groups of seven rats. Doses were chosen to cause similar increases in glomerular filtration rate (GFR). Time controls were included. 2. Glucagon raised GFR 32% and absolute proximal reabsorption (APR) 26% producing 81% effective proximal glomerulo-tubular balance (GTB) which was not significantly different from the 100% expected for perfect GTB. ANP raised GFR 33% and APR 10% indicating only 30% effective GTB (P less than 0.01). This was a significantly different effect from glucagon (P less than 0.005). 3. Sodium output increased 10-fold with ANP and 3-fold with glucagon. Filtration fraction increased 33% (P less than 0.04) above the pre-treatment value with ANP but was unchanged with glucagon. Plasma renin concentration was suppressed similarly by each hormone (46 and 36%, P less than 0.05, compared with pre-treatment values). 4. Despite a change in peritubular physical factors favouring reabsorption, there was almost complete attenuation of the increase expected in APR with the ANP-induced increase in GFR. In contrast, a similar change in GFR with glucagon resulted in an almost parallel increase in APR demonstrating maintenance of proximal GTB. 5. It is concluded that in the anaesthetized rat, ANP but not glucagon profoundly inhibits the increase in proximal reabsorption that normally follows an increase in filtered load. Such an action would contribute to the more potent natriuretic activity of ANP compared with glucagon.
 ...
PMID:The effects of atrial natriuretic peptide and glucagon on proximal glomerulo-tubular balance in anaesthetized rats. 297 22

In the present study we report methods for the isolation and culture of colonic peptide YY (PYY) cells and have tested the effects of sodium oleate and other chemotransmitters on PYY release. Enzyme-dispersed canine colonic mucosa cells were separated by a Beckman elutriation rotor, and the enriched PYY fraction was cultured on type I collagen in full growth medium. After 42-48 h of culture PYY cells had selectively adhered to the collagen. Forty to 45% of the adherent cells contained PYY (5.5 +/- 0.5 pmol/24-mm well), and 10-15% of the cells contained glucagon-like immunoactivity (GL29-LI; 0.95 pmol/24-mm well). The effect of various secretagogues on PYY release from these cultures was monitored. Sodium oleate stimulated PYY release in a time-dependent fashion over a dose range from 10 microM to 10 mM. However, sodium oleate at a dose of 100 mM produced disproportionately large PYY release. During a 2-h incubation 5.1% of the total cell content of PYY was released in response to 0.1 mM sodium oleate compared with basal release of 1.1%. At doses less than 10 mM sodium oleate did not release GL29-LI, whereas concentrations of 10 and 100 mM resulted in marked GL29-LI release. These findings suggest that lower concentrations of sodium oleate selectively release PYY, whereas higher concentrations nonselectively induce peptide release probably by effects on membrane stability. We also found that bombesin, epinephrine, and forskolin, but not carbachol, produced time- and dose-dependent release of PYY from these cultures.
 ...
PMID:Primary culture of PYY cells from canine colon. 337 82

The influence of Sodium-salicylate on insulin secretion and blood glucose behaviour was examined in 6 metabolic healthy persons and 9 type II-diabetics. Insulin secretion and blood glucose were twice examined under a combined stimulation with 100 g glucose (orally), 0.33 g glucose (Bolus injection) and 1.0 mg glucagon (i. v.) with and without a simultaneous infusion of Sodium salicylate during the whole period of examination (40 mg over 120 min). Sodium salicylate effected in type II-diabetics and metabolic healthy persons higher insulin levels. Qualitative differences of the insulin secretion pattern were not to be seen. In spite of higher insulin levels blood glucose was not influenced by Sodium salicylate. It is discussed if the results could be explained by a direct effect of Sodium salicylate on the cells ore on the metabolism of insulin and the gluconeogenesis.
 ...
PMID:[Effect of sodium salicylate on insulin secretion and blood glucose behavior in metabolically healthy and type II diabetic patients]. 391 57

We evaluated the effects of human calcitonin (hCT) on electrolyte excretion in hormone-deprived rats, that is, in the absence of endogenous parathyroid hormone, antidiuretic hormone, thyrocalcitonin and glucagon, the effects of which might have interfered with those of exogenous calcitonin. Plasma hCT levels, measured by radioimmunoassay, varied from 0 to 32 ng/ml. In these rats, hCT decreased magnesium (Mg) and calcium (Ca) excretion in a dose-dependent fashion. Maximal decreases were observed for hCT plasma concentrations comprised between 3 and 5 ng/ml, and persisted at the highest doses. Sodium, potassium, water, and total solute excretions were constant in the calcitonin concentration range explored. The same was observed for phosphate, except that slight but significant phosphaturia was elicited by the highest doses. Calcium and phosphate infusions to attenuate the fall in plasma Ca and phosphate concentration subsequent to hCT infusion, did not alter the hormonal effect on Ca and Mg excretion. hCT can therefore directly modulate Mg and Ca reabsorption by the kidney at plasma concentrations within the physiological range. The maximal effects on Mg and Ca reabsorption were obtained at plasma concentrations which are generally reached after maximal stimulation of endogenous calcitonin secretion. It is suggested that in rats, endogenous secretion of calcitonin stimulates Ca and Mg renal reabsorption without modification of sodium and phosphate excretion.
 ...
PMID:Modulation by calcitonin of magnesium and calcium urinary excretion in the rat. 399 91

Glucagon increases hepatocellular cAMP and decreases biliary cholesterol output. In these experiments, we examined the relation between cAMP and biliary cholesterol secretion. Bile flow and composition were measured in conscious dogs previously prepared by cholecystectomy, ligation of the lesser pancreatic duct, and placement of duodenal and gastric cannulae. Sodium taurocholate (500 mg/hr) was given intravenously to stabilize bile flow. After 2 hr of taurocholate infusion, dibutyryl cyclic AMP (160 mg kg-1 hr-1) or theophylline (20 mg kg-1 hr-1) was administered intravenously. Dibutyryl cAMP caused a decrease in both cholesterol concentration (242 +/- 25 micrograms/ml to 81 +/- 11 micrograms/ml) and cholesterol output (692 +/- 102 micrograms/15 min to 382 +/- 47 micrograms/15 min). Theophylline decreased cholesterol concentration (282 +/- 39 micrograms/ml to 221 +/- 21 micrograms/ml), but there was no significant change in cholesterol output. Bile flow increased significantly with both dibutyryl cAMP (2.8 +/- 0.2 ml/15 min to 4.9 +/- 0.2 ml/15 min) and theophylline (2.6 +/- 0.4 ml/15 min to 4.2 +/- 0.4 ml/15 min). In additional experiments, aminophylline (85% theophylline, 15% ethylenediamine) was administered intravenously (24.7 mg kg-1 hr-1). Aminophylline reduced cholesterol concentration (59 +/- 6 micrograms/ml to 36 +/- 5 micrograms/ml), but cholesterol output was stable. Bile flow increased significantly (3.7 +/- 0.2 ml/15 min to 6.5 +/- 0.4 ml/15 min). The mechanisms of these changes remain unknown. The effect of dibutyryl cAMP on biliary cholesterol secretion supports but does not prove the hypothesis that glucagon decreases biliary cholesterol output via the second messenger, cAMP.
 ...
PMID:Effects of dibutyryl cyclic AMP and theophylline on biliary cholesterol secretion. 631 85

Adult rat hepatocytes in primary culture were examined to determine if Na+-dependent transmembrane Ca2+ fluxes precede reinitiation of DNA synthesis. Studies with 45Ca2+ and atomic absorption measurements of 40Ca2+ showed that hepatocytes lack plasma membrane Na+-Ca2+ exchange activity. Under chemically defined conditions, combinations of mitogens - EGF, insulin, and glucagon - failed to induce transmembrane Ca2+ fluxes early in the prereplicative phase. In addition, a Ca2+ ionophore, A23187, was non-mitogenic. Thus, plasma membrane Na+-Ca2+ exchange is not a mitogenic signal for hepatocytes. Elevated intracellular Ca2+ levels are thought to mediate early prereplicative events required for animal cell proliferation. These conclusions stem partly from findings that A23187, a Ca2+ ionophore, stimulates transmembrane Ca2+ fluxes and proliferation in several cell systems (reviewed in Boynton et al., 1982). Sodium ion fluxes also are implicated as "initiating" mitogenic signals (Koch and Leffert, 1979). In particular, amiloride-sensitive Na+ influxes, stimulated by growth factors, may be necessary to initiate DNA synthesis in rat hepatocytes, mouse and human fibroblasts, rat liver derived cell lines, mouse sympathetic neurons, human lymphocytes, and monkey kidney epithelial cells (reviewed in Leffert, 1982). Several investigators, using cells from electrically excitable tissues (Schellenberg and Swanson, 1981; Eckert and Grosse, 1982), have reported that plasma membrane Na+-Ca2+ exchange carriers regulate intracellular Na+ and Ca2+ concentration. It is unclear if this exchange system exists in non-electrically excitable membranes, especially with regard to hepatocytes (Judah and Ahmed, 1964; van Rossum, 1970). We have here investigated the possible association of Na+ influxes with transmembrane Ca2+ movement following reinitiation of hepatocyte growth.
 ...
PMID:Initiation of cultured rat hepatocyte proliferation does not involve Na+-dependent plasma membrane Ca2+ fluxes. 632 28


1 2 3 4 5 6 Next >>