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

The effects of insulin on amino acid transport were studied in freshly prepared suspensions of isolated hepatocytes from adult rats. Insulin stimulated the active transport of alpha-aminoisobutyric acid by increasing the influx. The onset of the insulin effect was delayed by thirty to sixty min. Insulin increased by Vmax of transport by about 60% without affecting the Km. Cycloheximide and actinomycin D inhibited hormonal action by 60 to 80%. Only the "A" system of transport was affected by insulin. Half-maximal stimulation of transport was observed with insulin at 2 to 3nmol/l, a concentration which also occupies about 50% of insulin-specific binding sites at steady state. Insulin did not antagonize the stimulatory effect of glucagon on amino acid transport.
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PMID:Effect of insulin on amino acid transport in isolated rat hepatocytes. 70 Feb 71

Animal models with genetic or experimentally produced (lesions of hypothalamus) obesities are numerous and unlikely to ever be reduced to a single pathophysiologic entity. However, obese animals have many similar traits in common. They are all hyperinsulinemic, an abnormality that occurs early in the development of these syndromes and appears to be of prime importance in producing most of the metabolic changes observed both in the early and late phases of the obesity syndromes. In all instances, obesity is an evolutional syndrome in which the early phase is different from the later one. The early phase is principally characterized by increased hepatic very low density lipoprotein (VLDL) output, increased adipose tissue lipogenesis and VLDL uptake, hence, increased fat accretion and fat cell size. These abnormalities are secondary to hyperinsulinemia and can be reversed toward normal by normalizing circulating insulin levels. The late phase is characterized by the continuation of the disorders of the early one plus a superimposed abnormality, the insulin resistance state, that is detectable particularly at the level of adipose and muscle tissues, and eventually brings about hyperglycemia. Insulin resistance is a multifactorial pathological condition that includes at least: (a) a decrease (more or less marked) in insulin binding to target tissues that is responsible for the decrease in tissue sensitivity to the hormone; (b) intracellular defects that are probably responsible for the decreased insulin responsiveness of target tissues. The origin of hyperinsulinemia in animal obesities is still ill-defined. Lesions of the ventromedial hypothalamus (VMH) produce rapid and lasting hyperinsulinemia. Such lesions produce, in addition, increased secretion of insulin and glucagon and changes in pancreatic insulin, glucagon, and somatostatin content in subsequently perfused pancreases. The locus responsible for these effects is not defined and may actually involve a series of interrelated loci. Whatever the latter may be, one of the routes of CNS influence upon endocrine pancreas is the vagus nerve, although a humoral factor has also been claimed. The etiology of hyperinsulinemia in genetically obese animals is unknown. Genetic inheritance could bear primarily upon some hypothalamic or other CNS sites, with secondary alterations in the endocrine pancreas function, or primarily on the islets of Langerhans with possible alteration in the respective function of the A, B, and D cells with resulting excessive insulin secretion.
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PMID:Hyperinsulinemia in obesity syndromes: its metabolic consequences and possible etiology. 72 39

The effect of intravenous application of 1 mg glucagon on serum magnesium concentration, potassium, immunoreactive insulin (IRI), and blood glucose in healthy subjects has been studied. A significant decrease of the serum magnesium concentration was observed beginning 5 min after glucagon injection. There is a tendency of a slight but not statistically significant decrease of potassium level at 60 min. The beginning of the decrease of magnesium level was associated with the maximum of IRI-peak. In contrast to the discussed hypothesis that hyperglycemia and hyperinsulinemia cause a shift for magnesium and potassium from the extracellular into the intracellular space we could demonstrate that hyperglycemia is not a necessary condition for the decreasing effect of glucagon on serum magnesium level.
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PMID:Investigations on changes of serum magnesium concentration after glucagon application in healthy humans. 73 15

Hyperglycemia, hyperglucagonemia and hyperinsulinemia were observed in fasting rats at 0.5 hr after ip injection of NiCl2 (68 mumole per kg). Infusion of somatostatin iv (0.5 mg per rat) did not prevent Ni(II)-mediated hyperglycemia, hyperglucagonemia or hyperinsulinemia. Exposure of rats to inhalation of Ni(CO)4 (1.2 to 6.4 mumole per liter of air per 15 min) caused acute hyperglycemia, similar to that observed after ip injection of NiCl2. Hyperglycemia induced by NiCl2 and Ni(CO)4 was not associated with inhibition of erythrocyte glycolysis measured in vitro by erythrocyte uptake of 1-14C-glucose and release of 14CO2. These findings indicate that Ni-induced hyperglycemia may be mediated by increased pancreatic release of glucagon, but that Ni stimulation of glucagon release differs from stimulation of glucagon release by arginine or epinephrine, since the Ni effect is not antagonized by somatostatin.
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PMID:Effects of nickel chloride and nickel carbonyl upon glucose metabolism in rats. 73 12

Extreme hyperinsulinism was observed in endotoxin-shock dogs made hyperglycemic by glucose infusion. Qualitatively (at least in terms of gel filtration characteristics), the insulin secreted under these conditions was normal. Hyperinsulinism was not observed in endotoxin-shock dogs not given glucose. Thus hyperinsulinism does not explain the hypoglycemia so frequently observed in endotoxin-treated dogs. Hyperinsulinsm could not be impaired degradation of insulin as disappearance of labeled insulin as well as cold insulin was comparable in control and endotoxin-treated animals. An adrenergic mechanism (either beta receptor stimulation or postadrenergic hyperresponsiveness of the beta cells) probably does not explain the hyperinsulinism observed in endotoxin-shock dogs given glucose as beta blockade failed to inhibit the hyperinsulinsm. Hyperinsulinism was not observed in endotoxin-shock dogs given tolbuamide. A tenfold rise in plasma IRG was observed in endotoxin-treated dogs whether glucose was infused or not. The persistently low IRI levels in endotoxin-treated dogs not given glucose suggest that hyperresponsiveness of the beta cell to glucagon was not present in these animals. Extreme hyperinsulinsm in response to induced hyperglycemia in endotoxin-shock dogs is unexplained. Hyperresponsiveness of the beta cell to glucose during endotoxin shock seems likely.
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PMID:Hyperinsulinism in endotoxin shock dogs. 77 54

Most forms of liver disease are probably associated with impaired gluconeogenesis, although hypoglycaemia is rarely an important clinical feature. Blood concentrations of the gluconeogenic precursors, lactate, glycerol and alanine are elevated although, in certain situations, alanine levels may be decreased. Abnormal glucose tolerance is present in both acute and chronic liver disease, but is usually not of clinical importance. The mechanism of glucose intolerance remains uncertain, with diminished hepatocyte mass, portal diversion and insulin resistance the major postulates. Indeed, the importance of the liver in disposing of an oral glucose load, is still questioned. Both hyperinsulinism and hypoinsulinism are found in liver disease, with hyperinsulinism common in cirrhosis and acute viral hepatitis. This is accompanied by insulin resistance. The hyperinsulinism is probably due to defective hepatic clearance of insulin rather that to over-production. The cause of the insulin resistance remains to be established. Glucagon levels are raised and may contribute to this resistance. Growth hormone levels are also increased but are associated with low somatomedin levels and the role of growth hormone in insulin resistance is therefore questionable. Future developments include use of new animal models, studies of biopsy specimens and studies of hepatic hormone receptors.
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PMID:Carbohydrate metabolism in liver disease. 79 84

Glucose-glucagon relationships were examined in adult sheep. Hyperglycemia was induced by infusing glucose at 120 mg/hr/kg body weight. Hypoglycemia was obtained by infusing insulin at 1.2 U/hr. In several experiments glucose at 40 mg/hr/kg was infused with insulin to obtain hyperinsulinemia without hypoglycemia to distinguish glucose-insulin effects. Glucagon concentrations decreased during hyperglycemia and increased during hypoglycemia. This study indicates that glucose-glucagon interactions may be important in regulation of glucagon secretion in sheep.
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PMID:Glucose-glucagon relationships in adult sheep. 83 95

A system consisting of an isolated dog stomach perfused with whole blood has been designed to study gastric glucagon secretion. Under basal conditions, gastric glucagon release was 0.0-3.1 ng glucagon/100g of stomach per min. Arginine, at an arterial plasma concentration averaging 10 mM, elicited a rapid glucagon release. This gastric glucagon release was almost completely abolished by somatostatin (100 ng/ml). The release of gastric glucagon was not affected by hyperglycemia alone but was reduced by about 40% when hyperglycemia was concomitant with an hyperinsulinemia within the physiological range. These observations support the concept that adequate concentrations of insulin are necessary in order for hyperglycemia to inhibit gastric glucagon secretion. Furthermore, it is suggested that the isolated perfused dog stomach might provide a unique tool permitting investigation of alpha-cell function in the absence of endogenously released insulin.
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PMID:Factors controlling gastric-glucagon release. 84 58

The response of plasma insulin concentration to an oral glucose tolerance test (OGTT) and to the maximum stimulatory effect obtained with administration of glucose, glucagon and tolbutamide was studied in 24 siblings of diabetic children and in ten obese children. Five siblings of patients with diabetes sound to have chemical diabetes had hyperinsulinism during the OGTT. Serum insulin concentrations during the maximum stimulation of the beta cells in the children with chemical diabetes, although diminished at 15 minutes, were considered not significantly different from controls. Obese children had hyperinsulinism during the OGTT and the maximum stimulation of the beta cell. The data suggest that hyperinsulinism may precede or accompany carbohydrate intolerance in siblings of diabetic children.
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PMID:Maximum stimulation of insulin secretion in children with chemical diabetes and obesity. 94 38

Unidirectional K+ fluxes were measured in suspensions of isolated rat liver parenchymal cells incubated with 42K+ in vitro. By tracer exchange analysis fluxes in both directions were estimated to 8-9 10(-12) mol/cm2. Glucagon in concentrations above 2 x 10(-8) M increased both influx and efflux to 160% of control values. Insulin increased influx by 12-14%, whereas efflux was apparently unaffected. Using an extracellular marker 51Cr EDTA, intracellular level of some ions was estimated in isolated liver cells: K+ = 172 mmol/kg water, Na+ = 25 mmol/kg water, Cl = 53 mmol/kg water. Cellular water content: 60%. Incubation with insulin for 1 h increased the intracellular concentration of K+ 1.7 mmol/kg water. The results indicate that glucoagon increased primarily the K+-permeability of the cell membrane, while insulin stimulates active K+ transport into the cell.
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PMID:K+ transport in isolated rat liver cells stimulated by glucagon and insulin in vitro. 94 6


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