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 purpose of this study was to determine if the changes in selected blood hormones and substrates, metabolic rate, and rectal temperature (Tre) in nine males after immersion in 10 degrees C water, while clad in standard flight suits, were related to the level of aerobic fitness. Fitness was evaluated by the blood lactate response to submaximal exercise. Immersion time (IT) was defined as the time required for a 1 degrees C decrease in Tre and averaged 38.5 (range: 21-62) min. Metabolic rate increased 3.4 times the resting rate. Lactate, free fatty acids, triiodothyronine and thyroxine increased by 81%, 38%, 11%, and 8%, respectively, in contrast to insulin which decreased by 32%, with all changes being statistically significant (p less than 0.05). Glucagon increased slightly but not significantly (p = 0.11) while glucose levels did not change. The IT was correlated directly with a measure of aerobic fitness, with relative body fat, and with the T3 levels postimmersion (p less than 0.05). The results suggest that the aerobic fitness level can significantly influence the cooling rate during water immersion.
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PMID:Effects of endurance fitness on responses to cold water immersion. 648 7

Isolated liver cells from rats fed a diet deficient in essential fatty acids were used to study the oxidation, esterification and, especially, the desaturation and chain elongation of [1-14C]linoleic acid. 14C-labelled arachidonic acid (20:4) and smaller amounts of eicosatrienoic acid (20:3) were recovered mainly in the phospholipids, while gamma-linolenic acid (18:3) was found in both the phospholipids and the triacylglycerol fraction. Lactate strongly increased the formation of arachidonic acid, which was found mainly in the phosphatidylcholine and the phosphatidylinositol fractions. Lactate reduced the amounts of gamma-linolenic acid. Glucagon and (+)-decanoylcarnitine reduced the formation of arachidonic acid, and (+)-decanoylcarnitine increased the incorporation of gamma-linolenic acid especially, in the triacylglycerol fraction. Increasing concentrations of the [1-14C]linoleic acid substrate increased the formation of arachidonic acid and of the other chain-elongated or desaturated fatty acids. Lactate also stimulated the formation of arachidonic acid in liver cells from animals fed adequate amounts of essential fatty acids. It is suggested that dietary and hormonal factors which can change the intracellular levels of malonyl-CoA may influence both the ratio of arachidonic acid/gamma-linolenic acid formed and the total amounts of desaturated and chain-elongated fatty acids formed from linoleic acid.
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PMID:Studies on the regulation of arachidonic acid synthesis in isolated rat liver cells. 681 39

The metabolic and hormonal consequences of long term intravenous insulin replacement were studied in 11 pancreatectomised dogs. Insulin was delivered into the portal circulation of six animals for 164-224 days and into the peripheral circulation of the remainder for 123-365 days. Infusion rates were initially adjusted to achieve normoglycaemia in the fasting (0.37 +/- 0.01 mU Kg-1 min-1 portal; 0.45 +/- 0.03 mU kg-1 min-1 peripheral) and post-prandial states (2.57 +/- 0.07 mU kg-1 min-1 for 7 1/2 h portal; 3.16 +/- 0.18 mU kg-1 min-1 for 7 h peripheral). Animals were fed their usual mixed diet and blood samples were drawn from indwelling catheters at regular intervals for 24 h. A matched group of six normal dogs was similarly studied. Significantly less insulin was needed for glycaemic normalisation with portal (1.05 +/- 0.03 U kg-1 day-1) compared with peripheral (1.27 +/- 0.08 U kg-1 day-1) infusions, but post-prandial insulin levels were not normalised. Glucagon levels were normal and unaffected by the route of insulin infusion. Lactate and pyruvate responses were exaggerated post-prandially in the diabetic compared with the normal dogs. Fasting non-esterified fatty acid levels were suppressed with peripheral but normal with portal insulin infusion. There were only minor differences in the branched chain, essential and other non-essential amino acids except for alanine which was significantly above normal in the diabetic animals. Fasting levels of insulin, lactate, pyruvate and non-esterified fatty acids were normalised only with portal infusion while glucose, glucagon, 3-hydroxybutyrate and most amino acids were normalised regardless of the route of infusion. We conclude that the metabolic regulation achieved with portal insulin replacement is closer to normal than that achieved with peripheral infusion.
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PMID:The metabolic and hormonal responses to a mixed meal in unrestrained pancreatectomised dogs chronically treated by portal or peripheral insulin infusion. 702 31

The facilitation of glucose disposal (Staub-Traugott effect) and potentiation of serum insulin (IRI) concentration normally occurring after closely spaced intravenous glucose loads, are known to disappear after prolonged starvation. To study the effects of minimal amounts of glucose during fasting upon the insulin response and disposal of repeated intravenous glucose tolerance tests, obese volunteers were fasted for a mean of 25 +/- 2 days, while receiving either 8 or 16 gm of oral glucose every 6 hr, and compared to totally fasted subjects without glucose supplementation. Weight loss rate and the fall in basal IRI and glucose levels were similar to those of totally fasted subjects. However, the Staub-Traugott effect and insulin secretory dynamics after stimulation by repetitive intravenous glucose loading were preserved by this glucose modified fast, while baseline serum glucagon levels (IRG) were significantly lower, and the basal IRI/IRG ratios were thus unchanged from the fed state. IRG and free fatty acid suppression were similar in the fed and glucose modified fasted states. Lactic acid levels increased as expected after the repeated glucose injections in the fed state, but failed to do so after the prolonged modified fast until the second and third repetitive glucose loads, in which a significant rise coincided with accelerated glucose disposal. It is suggested that minimal amounts of carbohydrate during fasting preserve the insulin potentiating action of glucose, preferentially sparing a delayed releasable pool of insulin, while protecting the glucose utilization mechanisms, including increased glycolysis, responsible for the Staub-Traugott effect.
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PMID:Preservation of glucose tolerance and insulin secretory response to repeated glucose levels by the feeding of minimal glucose during prolonged fasting. 703 19

Hepatocyte monolayers were established from young preruminating (7 to 14 d of age) or older ruminating (11 to 12 wk of age) calves and used to evaluate the effects of insulin and glucagon on incorporation of carbon from 2.5 mM [2-14C]propionate and 2.0 mM [U-14C]lactate into glucose and glycogen. Developmental state (young preruminating vs older ruminating) of the donor calf did not affect the rate of gluconeogenesis from propionate in the absence of hormones. Insulin decreased (P < .05) gluconeogenesis and increased (P < .05) glycogenesis from propionate and lactate in hepatocytes from preruminating calves but had no effect on hepatocytes from ruminating calves. Lactate was poorly metabolized to glucose and was not responsive to glucagon in hepatocytes from ruminating calves compared with hepatocytes from preruminating calves. Hepatocytes responded to glucagon by increasing (P < .05) gluconeogenesis from propionate. Maximal responsiveness to glucagon did not differ between ruminating and preruminating calves, but hepatocytes from preruminating calves responded at lower glucagon concentrations (P < .05). These data demonstrate a similar capacity of hepatocytes from preruminating and ruminating calves to metabolize propionate to glucose, but there was a seven- to eightfold decrease in gluconeogenesis from lactate in ruminating calves that was accompanied by a decreased response to acute changes in insulin and glucagon.
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PMID:Insulin and glucagon regulation of gluconeogenesis in preruminating and ruminating bovine. 760 89

Severe hypoglycaemia with brain dysfunction limits intensified therapy in patients with insulin-dependent diabetes mellitus, despite evidence that such therapy reduces the risk of chronic complications of the disease. We have investigated the effect of infusing lactate (a potential non-glucose fuel for brain metabolism) on protective, symptomatic neurohumoral responses and on brain function during hypoglycaemia in seven healthy men. Elevation of lactate (within a physiological range) substantially diminished catecholamines, growth hormone, cortisol, and symptomatic responses to hypoglycaemia and lowered the glucose level at which these responses began. Glucagon responses were unaffected. Lactate was also associated with a significant lowering of the glucose level at which brain function deteriorated, suggesting that brain function was protected during the hypoglycaemia. The defect in counter-regulation is similar to that seen in hypoglycaemia-prone diabetic patients. Initiation of the protective responses to hypoglycaemia (except glucagon) can be delayed by supporting metabolism with an alternative metabolic fuel. Cerebral cortical dysfunction of severe hypoglycaemia is also delayed. Our demonstration that higher brain function can be protected during hypoglycaemia may have therapeutic potential.
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PMID:Protection by lactate of cerebral function during hypoglycaemia. 790 61

The effects of neuroleptanaesthesia on endocrine-metabolic changes during elective gastrectomy was investigated, comparing with those of epidural anaesthesia. Nine patients were given neuroleptanaesthesia and fifteen patients given thoracic epidural analgesia combined with general anaesthesia. We evaluated the levels of stress hormones, insulin and blood glucose. Epidural anaesthesia suppressed the increase of catecholamine, but neuroleptanaesthesia did not inhibit the elevation of the catecholamines. In neuroleptanaesthesia group, glucagon and growth hormone increased during surgery, and the levels of these hormones were significantly higher than those of epidural analgesia group. Blood glucose increased during operation in both groups. In epidural anaesthesia, the levels of insulin and insulin/glucose ratio were kept higher than those of neuroleptanaesthesia group, but this was not statistically significant. Lactate/pyruvate ratio and free fatty acid did not show any significant change during the study in both groups. These results suggest that neuroleptanaesthesia is not a suitable method for upper abdominal surgery.
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PMID:[Effect of neuroleptanaesthesia on endocrine-metabolic response during upper abdominal surgery]. 816 18

Hepatocyte monolayers from neonatal calves were used to determine the effects of glucagon and insulin on incorporation of carbon from [2-14C]propionate, [1-14C]lactate, [U-14C]lactate, and [1,3-14C]glycerol into glucose and glycogen. Glucagon increased gluconeogenesis (nmol substrate incorporated into glucose or glycogen.micrograms DNA-1.h-1) from propionate and lactate but not from glycerol. Insulin decreased gluconeogenesis from [2-14C]propionate but was without effect on gluconeogenesis from [U-14C]lactate or [1,3-14C]glycerol. Net de novo glycogenesis (nmol substrate retained in cell glycogen.micrograms DNA-1.h-1) from propionate, lactate, and glycerol was decreased by glucagon and increased by insulin. Glucagon effects on gluconeogenesis, but not glycogenesis, were mimicked by dibutyryl adenosine 3',5'-cyclic monophosphate. Lactate flux through pyruvate carboxylase accounts for > or = 91% of lactate carbon flux to glucose, and this proportion was unchanged by glucagon or insulin. Gluconeogenesis from propionate and lactate is regulated by substrate concentration and glucagon in bovine hepatocyte monolayers. The data indicate that, in neonatal bovine liver, glucagon acts on a process common to lactate and propionate to increase gluconeogenesis, and insulin opposes these effects on gluconeogenesis from propionate but not lactate.
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PMID:Regulation of gluconeogenesis by insulin and glucagon in the neonatal bovine. 818 66

The short- and long-term effects of simultaneous administration of terbutaline and betamethasone were investigated in 8 gravidas treated for preterm labor. Their plasma concentrations of glucose, insulin, glucagon, C-peptide, lactate and potassium were compared to a control group receiving intravenous magnesium sulfate and betamethasone. The patients on terbutaline therapy had a marked hyperglycemia at 11 h which remained elevated for 48 h. There was a simultaneous rise in plasma insulin and C-peptide, and a fall in plasma glucagon. Lactate levels were markedly elevated. Only 1 of the 8 patients had an abnormal glucose tolerance test at 1 week of therapy. The metabolic changes of control patients were minimal in comparison and there was no lacticacidemia. This suggests that glucocorticoids potentiate the hyperglycemic response of terbutaline.
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PMID:Combined effect of terbutaline and betamethasone on glucose homeostasis in preterm labor. 824 Jun 92

The release of glucokinase from digitonin-permeabilized hepatocytes shows different characteristics with respect to ionic strength and [MgCl2] from the release of other cytoplasmic enzymes. Release of glucokinase is most rapid at low ionic strength (300 mM sucrose, 3 mM Hepes) and is inhibited by increasing concentration of KCl [concn. giving half-maximal inhibition (I50) 25 mM] or Mg2+ (I50 0.5 mM). Release of phosphoglucoisomerase, phosphoglucomutase and glucose-6-phosphate dehydrogenase is independent of ionic strength, but shows a small inhibition by MgCl2 (20%, versus > 80% for glucokinase). Lactate dehydrogenase release increases with increasing ionic strength [concn. giving half-maximal activation (A50) 10 mM KCl] or [MgCl2]. The rate and extent of glucokinase release during permeabilization in 300 mM sucrose, 5 mM MgCl2 or in medium with ionic composition resembling cytoplasm (150 mM K+, 50 mM Cl-, 1 mM Mg2+) depends on the substrate concentrations with which the hepatocytes have been preincubated. In hepatocytes pre-cultured with 5 mM glucose the release of glucokinase was much slower than that of other cytoplasmic enzymes measured. However, preincubation with glucose (10-30 mM) or fructose (50 microM-1 mM) markedly increased glucokinase release. This suggests that, in cells maintained in 5 mM glucose, glucokinase is present predominantly in a bound state and this binding is dependent on the presence of Mg2+. The enzyme can be released or translocated from its bound state by an increase in [glucose] (A50 15 mM) or by fructose (A50 50 microM). The effects of glucose and fructose were rapid (t1/2 5 min) and reversible, and were potentiated by insulin and counteracted by glucagon. They were inhibited by cyanide, but not by cytochalasin D, phalloidin or colchicine. Mannose had a glucose-like effect (A50 approximately 15 mM), whereas galactose, 3-O-methyl-D-glucose and 2-deoxyglucose were ineffective. When hepatocytes were incubated with [2-3H, U-14C]glucose, the incorporation of 3H/14C label into glycogen correlated with the extent of glucokinase release. Since 2-3H is lost during conversion of glucose 6-phosphate into fructose 6-phosphate, substrate-induced translocation of glucokinase from a Mg(2+)-dependent binding site to an alternative site might favour the partitioning of glucose 6-phosphate towards glycogen, as opposed to phosphoglucoisomerase.
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PMID:Intracellular binding of glucokinase in hepatocytes and translocation by glucose, fructose and insulin. 828 78


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