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)

The effect of increased endogenous plasma insulin and glucagon concentrations on the free fatty acid (FFA) levels in the circulating blood was investigated in sheep, 2 baboons and 1 vervet monkey. Elevation of the plasma insulin level was obtained by vagal stimulation or intravenous glucose administration and vagal stimulation, whereas increased glucagon levels were induced by sympathetic stimulation, increased plasma insulin levels, with simultaneous increased plasma glucose concentrations (in our experiments with sheep), produced a pronounced lowering of the FFA levels. From this observation a lipogenetic function could be ascribed to insulin. However, in the primate experiments, increased plasma insulin without concomitant glucose administration caused an elevation of FFA levels, and would indicate a lipolytic rather than a lipogenetic action of insulin. Increased glucagon levels, as produced by sympathetic stimulation, did not alter the FFA concentrations significantly. It thus appears that glucagon has no lipolytic effect, as claimed by previous investigators. In our experiment on the vervet monkey, sympathetic stimulation, with increased plasma glucagon, even caused a decrease in FFA levels.
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PMID:[The influence of endogenous insulin and glucagon on the free fatty acids in the circulating blood plasma]. 11 97

Changes in plasma glucose, nonesterified fatty acids, insulin, glucagon, cortisol, growth hormone, and prolactin have been studied in baboons during the course of generalized epileptic seizures induced by intravenous bicuculline. Plasma glucose rose to a peak at 25 min but fell to hypoglycemic levels after 60 min of seizure activity. This hypoglycemia was accompanied by a marked elevation in plasma insulin. Plasma glucagon rose to a peak at 14 min, then returned to normal. Plasma growth hormone levels were elevated after 60 min of seizure activity. Plasma prolactin and cortisol levels also rose during the seizure. These changes result from sequential interaction of (1) autonomic activation at seizure onset, (2) spread of neuronal activity to the hypothalamus leading to the liberation of releasing factors, and (3) indirect physiologic consequences of seizure activity.
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PMID:Endocrine factors and glucose metabolism during prolonged seizures in baboons. 11 9

1. Hepatocytes from starved rats or fed rats whose glycogen content was previously depleted by phlorrhizin or by glucagon injections, form glycogen at rapid rates when incubated with 10mM-glucose, gluconeogenic precursors (lactate, glycerol, fructose etc.) and glutamine. There is a net synthesis of glucose and glycogen. 14C from all three types of substrate is incorporated into glycogen, but the incorporation from glucose represents exchange of carbon atoms, rather than net incorporation. 14C incorporation does not serve to measure net glycogen synthesis from any one substrate. 2. With glucose as sole substrate net glucose uptake and glycogen deposition commences at concentrations of about 12--15mM. Glycogen synthesis increases with glucose concentrations attaining maximal values at 50--60mM, when it is similar to that obtained in the presence of 10mM glucose and lactate plus glutamine. 3. The activities of the active (a) and total (a+b) forms of glycogen synthase and phosphorylase were monitored concomitant with glycogen synthesis. Total synthase was not constant during a 1 h incubation period. Total and active synthase activity increased in parallel with glycogen synthesis. 4. Glycogen phosphorylase was assayed in two directions, by conversion of glycose 1-phosphate into glycogen and by the phosphorylation of glycogen. Total phosphorylase was assyed in the presence of AMP or after conversion into the phosphorylated form by phosphorylase kinase. Results obtained by the various methods were compared. Although the rates measured by the procedures differ, the pattern of change during incubation was much the same. Total phosphorylase was not constant. 5. The amounts of active and total phosphorylase were highest in the washed cell pellet. Incubation in an oxygenated medium, with or without substrates, caused a prompt and pronounced decline in the assayed amounts of active and total enzyme. There was no correlation between phosphorylase activity and glycogen synthesis from gluconeogenic substrates. With fructose, active and total phosphorylase activities increased during glycogen syntheses. 6. In glycogen synthesis from glucose as sole substrate there was a decline in phosphorylase activities with increased glucose concentration and increased rates of glycogen deposition. The decrease was marked in cells from fed rats. 7. To determine whether phosphorolysis and glycogen synthesis occur concurrently, glycogen was prelabelled with [2-3H,1-14C]-galactose. During subsequent glycogen deposition there was no loss of activity from glycogen in spite of high amounts of assayable active phosphorylase.
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PMID:Glycogen synthesis by rat hepatocytes. 11 69

Chronic renal failure results in a variety of metabolic derangements that perturb glucose homeostasis. These may in part result from the fact that the kidney plays a prominent role in the metabolism of insulin as well as a number of other low-molecular-weight peptide hormones that affect carbohydrate metabolism. Specific abnormalities in glucose utilization that appear to be related to alterations in membrane receptors, resulting in increased glucagon sensitivity and decreased insulin action, are a newly recognized factor in intolerance to oral glucose. Glucose production and utilization are both abnormally increased in patients with chronic uremia, and these disturbances are only partially corrected by hemodialysis treatment. The mechanism(s) contributing to these changes is unclear, but seems to involve a combination of humoral and cellular factors. These include some degree of insulin resistance, probably inadequately modulated proteolytic responses to glucagon and parathyroid hormone, and a basic defect in energy production that alters intracellular concentrations of high-energy phosphate-containing nucleotides. It is unclear whether these changes in carbohydrate tolerance pose an increased risk for the premature development of cardiovascular disease in patients with renal failure, as they appear to do in the nonuremic population. The occasional patient with renal failure may develop clinical hypoglycemia when glucose utilization continues in a setting in which the hepatic capacity to produce glucose is reduced, probably as a consequence of altered substrate delivery and/or inhibition of one or more key gluconeogenic enzymes.
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PMID:Disorders of glucose metabolism in uremia. 11 52

Glibenclamide has been shown to stimulate an insulin releasing factor in the duodenum. The possibility that this effect is of importance in its hypoglycaemic action was investigated by studying the effect of galactose on insulin release before and after treatment with glibenclamide; galactose stimulates insulin release when given orally but has no effect when given parenterally; thus its ability to release insulin appears to reside in an action on a gut factor. Measurements of plasma glucose, insulin and glucagon were made on twelve maturity onset diabetic patients following an oral glucose tolerance test and an oral galactose tolerance test before and after one week of treatment with glibenclamide. Glibenclamide significantly reduced the blood glucose levels. Both basal insulin and basal glucagon levels were unchanged. The insulin response to oral glucose was enhanced. Glucagon levels before treatment did not suppression of glucagon levels. Galactose stimulated insulin release but insulin levels before and after treatment were identical. An effect of glibenclamide on gut insulin releasing activity was not demonstrated but the galactose tolerance test provides a useful technique by which to examine the enteroinsular axis.
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PMID:The effect of glibenclamide treatment on the insulin and glucagon responses to oral glucose and galactose in maturity onset diabetics. 11 30

Glucose tolerance and insulin and glucagon secretion were examined sequentially during 6 months of calorie and carbohydrate restriction in an obese, recent-onset, ketosis-resistant diabetic adult. The subject was then followed for 9 additional months, during which some weight was regained. Fasting plasma glucose levels returned to normal after 6 week of calorie restriction and remained normal during periods of carbohydrate refeeding. Normalization of 2-h plasma glucose concentrations after a standard oral carbohydrate load required 5 months, and glucose disposal after an iv glucose load did not return to normal until the end of the study. Insulin secretion in response to oral glucose reached maximal levels during the first months of weight reduction and then decreased as glucose tolerance continued to improve. Acute phase insulin release in response to iv glucose gradually increased throughout the study. Glucagon stimulation by iv arginine and suppression by iv glucose also returned to normal levels slowly over several months. Abnormalities in glucose tolerance and glucoregulatory hormone secretion of ketosis-resistant diabetes are totally reversible with prolonged dietary therapy. Reduction in tissue resistance to the action of insulin also appeared to be of major importance in the recovery of normal glucose tolerance in this subject.
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PMID:Normalization of insulin and glucagon secretion in ketosis-resistant diabetes mellitus with prolonged diet therapy. 11 19

The effect of a sulfonylurea, glibenclamide, on the release of insulin, glucagon, and somatostatin was studied in the isolated perfused rat pancreas. At glucose concentrations of 1.1 mM or less, the drug stimulated somatostatin release, whereas glucagon release, after 2-3 min of increase, was markedly inhibited. Insulin release was moderately stimulated, and maximal release occurred relatively late. A moderate glucose load (6.7 mM) inhibited glibenclamide-induced release of somatostatin, whereas the two in combination exerted an additive action on insulin release. Greater glucose loads, which by themselves would stimulate somatostatin release, only marginally suppressed glibenclamide-induced somatostatin release. The insulinogenic effect of these glucose levels was not modified by glibenclamide. Glibenclamide may thus stimulate both the alpha and beta as well as delta cells of the pancreas, depending on glucose concentration. We suggest a paracrine (local) interaction of somatostatin with the alpha and beta cells, which has an important role in the kinetics of insulin and glucagon release induced by sulfonylureas.
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PMID:Effect of glucose/sulfonylurea interaction on release of insulin, glucagon, and somatostatin from isolated perfused rat pancreas. 11 58

Two groups (each of 6 moderately ill, protein-depleted patients) were infused daily for 7 days. Mean 7 day nitrogen (N) balances with infusions of 0.83 and 1.83 g of a defined amino acid mixture (containing further nutrients but no other source of energy)/kg ideal body wt/day were -3.66 and +1.54 g/day, respectively (P less than 0.025) when adjusted for changes in body urea and estimated miscellaneous N losses. Concentrations of plasma free fatty acids, immunoreactive insulin and glucagon, and of blood glucose, pyruvate, lactate and glycerol were indistinguishable on corresponding treatment days in the 2 groups but blood ketone bodies were lower in the 1.83 g/kg group. Blood amino acid concentrations of alanine, valine, leucine, and isoleucine were similar, whereas those of phenylalanine, histidine, serine, and arginine were higher, and glutamine lower, in the 1.83 g/kg group. The data confirm that not only can body protein mass be maintained, but a net positive N retention achieved, in such patients, through provision of exogenous amino acids and concurrent mobilization of endogenous energy stores. Of note is that this fat mobilization can occur without plasma free fatty acids and/or significant blood ketone body elevations. An infusion of 2, rather than 1 g/kg/day seems suitable in the situation examined.
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PMID:Intravenous protein-sparing therapy in patients with gastrointestinal disease. 11 60

Gliquidone (a second generation sulphonylurea) was administered orally to normal rats 1 h before killing. Gliquidone treatment led to a decrease in plasma glucose, an increase in insulin and a diminution in glucagon concentration. Insulin binding to liver plasma membranes was enhanced by 40% in comparison with controls, whereas glucagon binding was slightly diminished. These findings indicate a greater sensitivity of liver cells to insulin during sulphonylurea treatment and support the view that sulphonylureas potentiate insulin action on the liver.
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PMID:Extrapancreatic action of sulphonylureas: effect of gliquidone on insulin and glucagon binding to rat liver plasma membranes. 11 39

1. Frog liver has enzymatic systems able to interconvert glycogen synthase. 2. D to I conversion is achieved in vitro by incubation at 30 degrees C. ATP, ADP, inorganic phosphate and glycogen are inhibitors of this conversion, whereas glucose-6-P and Mg2+ stimulate it. 3. I to D conversion in vitro depends on ATP-Mg2+. Cyclic-AMP activates this conversion, while glucose-6-P inhibits it. 4. Injection of glucose, ribose, mannose, fructose, galactose, and cortisone into frogs increase liver percentage of I activity. 5. Glucagon and adrenaline decrease percentage of I activity.
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PMID:Frog liver glycogen synthase. In vitro and in vivo interconversions between I and D forms. 12 65


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