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)

1. The effect of acetate absorbed from the gut on glucose turnover has been determined in four healthy subjects during both fasting and an intravenous glucose infusion by using [U-13C]glucose. 2. In the first part of the study, after an overnight fast, a tracer dose of [U-13C]glucose was infused at a constant rate along with an infusion of saline for 7 h. In the second part the saline infusion was replaced by glucose at 4.25 mg min-1 kg-1. In both studies 15 mmol of sodium acetate was given by mouth at 15 min intervals from the fourth to the sixth hour. Glucose turnover, respiratory quotient, metabolic rate and blood levels of acetate, 3-hydroxybutyrate, lactate, insulin, glucagon and gastric inhibitory polypeptide were measured. 3. Glucose turnover rates (means +/- SEM) were 1.88 +/- 0.1 mg min-1 kg-1 during fasting and 4.0 +/- 0.08 mg min-1 kg-1 during glucose infusion. Acetate had no effect on glucose turnover, insulin, glucagon and gastric inhibitory polypeptide levels, but temporarily halted the rise in free fatty acids seen during the fasting study. No changes in oxygen consumption or carbon dioxide output occurred, in keeping with previous observations that acetate substitutes for lipid oxidation during metabolism and has no direct effect on glucose turnover.
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PMID:Effect of gut-derived acetate on glucose turnover in man. 284 53

In rat hepatocytes, vanadate increases fructose 2,6-bisphosphate (Fru-2,6-P2) in a time- and dose-dependent manner, and counteracts the decrease in this metabolite caused by glucagon, forskolin or exogenous cyclic AMP. Vanadate does not directly modify the activity of 6-phosphofructo-2-kinase, even though it can counteract the inactivation of this enzyme caused by glucagon. Furthermore, vanadate raises the yield of 3H2O from [3-3H]glucose, indicating that it increases the flux through 6-phosphofructo-1-kinase. Moreover, vanadate in hepatocytes incubated in the presence of glucose increases the production of both lactate and CO2. Therefore vanadate has insulin-like effects on the glycolytic pathway in rat hepatocytes. These results clearly contrast with our previous observation that vanadate exerts glycogenolytic non-insulin-like effects on glycogen synthase and phosphorylase.
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PMID:Vanadate raises fructose 2,6-bisphosphate concentrations and activates glycolysis in rat hepatocytes. 284 17

Early metabolic and endocrine changes in calves in response to two beta-adrenoceptor agonists in the absence and presence of the beta-adrenoceptor blocking agent propranolol have been studied in calves. The agonists were administered p.o. with milk in different amounts, whereas propranolol was infused i.v. for 10 h. Respiration volume, O2 consumption, CO2 production, respiratory quotient, blood glucose, lactate, non-esterified fatty acids and insulin transiently increased within 2-4 h in a dose-dependent manner, whereas glucagon, adrenaline, noradrenaline, triiodothyronine, urea, albumin and protein did not change significantly. Propranolol completely inhibited the effects on glucose, lactate, non-esterified fatty acids and insulin. Six hours after the administration of the beta-adrenoceptor agonists, the glucose clearance rates following i.v. infusion of glucose were markedly reduced and the glucose decrements in response to an i.v. injection of insulin were much smaller than in the absence of the beta-adrenoceptor agonists. The metabolic changes demonstrate an enhanced glycogenolysis and fat mobilisation, an increased metabolic rate and the development of insulin resistance within 6 h after the administration of the beta-adrenoceptor agonists.
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PMID:Early metabolic and endocrine effects of perorally administered beta-adrenoceptor agonists in calves. 290 69

We evaluated the effects of dopamine (DA) and synthetic atrial natriuretic polypeptide (ANP) on the release of catecholamines (CA) from the adrenal medulla. Adrenal glands of male Wistar rats were superfused with Ringer's solution saturated with 95%, O2, 5% CO2 by the use of a continuous flow incubation system, and norepinephrine (NE) and epinephrine (E) concentrations in the perfusate were continuously measured by high pressure liquid chromatography with fluorescent reaction. And the effects of DA and ANP on the CA release were evaluated. Next the effects of metoclopramide (MC), dopamine (D2) antagonist, and glucagon were added in the Ringer's solution, and the changes of NE and E in the perfusate were determined. Basal secretion of NE and E were 0.02-0.04 ng/mg.wet weight/min and 0.05-0.1 ng/mg.wet weight/min, respectively. DA remarkably decreased both NE and E release, and the suppressive effect was dependent on DA concentration in the perfusate. MC clearly raised NE and E release as well as glucagon. The increasing effect of MC was perfectly suppressed by 10(-4) M of DA. But the effect of glucagon was not blocked by the same dose of DA. Alpha rANP (10(-5)M) slightly decreased the releases of NE and E from adrenal medulla, and the magnitude of the effect of rANP was smaller than that of DA. MC significantly increased NE and E release even when the adrenal gland was superfused with Ringer's solution containing 10(-5)M of rANP. These data suggest that the release of CA from adrenal medulla may be regulated by DA, and that the receptors specifically binding to DA may exist in adrenal medulla as well as sympathetic presynaps. We concluded that DA (but not ANP) may play an important role in controlling (suppressing) the activity of sympathoadrenomedullary system.
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PMID:[Effects of dopamine and synthetic atrial natriuretic polypeptide on the release of norepinephrine and epinephrine from the adrenal medulla of rats]. 296 May 68

The effect of short-term (8-10 days) optimal glycaemic control achieved by continuous subcutaneous insulin infusion on resting energy expenditure and food-induced thermogenesis was studied. Oxygen consumption and carbon dioxide production were measured by indirect calorimetry in six newly-diagnosed and six chronically-treated diabetic children before and following the consumption of a standardized test meal. The metabolic and hormonal responses to the test meal and nutrient utilization were also assessed and compared with those measured in nine non-diabetic children. The restoration of normoglycaemia was accompanied by hypoglucagonaemia, hypoketonaemia, increased insulin:glucagon ratio and abnormal postmeal fall in free fatty acid levels in spite of normal fasting and post-prandial plasma free insulin levels. These changes suggesting increased insulin action were most pronounced in newly-diagnosed diabetic children. Possibly as a result of increased insulin action high carbohydrate, low fat utilization and increased food-induced thermogenesis were observed in the newly-diagnosed diabetic children. In the chronically-treated group these parameters were approaching the normal. Resting energy expenditure was normal in both groups of diabetics. These findings suggest that precise glycaemic control can be achieved only at the expense of some degree of peripheral hyperinsulinisation which leads to altered nutrient utilization and food-induced thermogenesis in the newly-diagnosed diabetic children.
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PMID:Resting energy expenditure and food-induced thermogenesis in diabetic children receiving continuous subcutaneous insulin infusion. 304 18

The effects of ethanol administration on activity and regulation of carnitine palmitoyltransferase I (CPT-I) were studied in hepatocytes isolated from rats fed a liquid, high-fat diet containing 36% of total calories as ethanol or an isocaloric amount of sucrose. Cells were isolated at several time points in the course of a 5-week experimental period. Ethanol consumption markedly decreased CPT-I activity and increased enzyme sensitivity to inhibition by exogenously added malonyl-CoA. Changes in enzyme activity occurred sooner than those in enzyme sensitivity. Fatty acid oxidation to CO2 and ketone bodies was depressed in hepatocytes from ethanol-fed animals during the first part of the treatment. At the end of the 35-day period, there were no longer differences in the rate of ketogenesis between the two groups. At that time, however, the rate of CO2 formation was still impaired in the ethanol-fed animals. Furthermore, addition of ethanol or acetaldehyde to the incubation medium strongly depressed CPT-I activity and rates of fatty acid oxidation in hepatocytes from ethanol-treated rats, whereas these effects were much less pronounced in cells from control animals. The response of CPT-I activity to insulin, glucagon, vasopressin, and phorbol ester was blunted in cells derived from ethanol-fed rats. These changes in the regulation of CPT-I activity corresponded with those observed in the rate of fatty acid oxidation. It is concluded that CPT-I may play a role in the generation of the ethanol-induced fatty liver.
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PMID:Effects of ethanol feeding on the activity and regulation of hepatic carnitine palmitoyltransferase I. 306 12

Sepsis and trauma result in increases in epinephrine, glucagon, and cortisol secretion as well as alterations in respiratory pattern that is characterized by increased minute ventilation, decreased tidal volume, and increased frequency. Six male subjects were infused for 5.5 hours with cortisol, epinephrine, and glucagon in amounts designed to simulate plasma levels seen in patients following trauma. During the initial 20 minutes of the hormone infusion, minute ventilation (VE), oxygen consumption (VO2), and carbon dioxide production (VCO2) increased above preinfusion values. VCO2 increased more than VO2 resulting in an increase in respiratory quotient (RQ) from 0.93 to 1.14. The increase in VE was due to increased tidal volume and not frequency (f). After 4.5 hours, the VE, VO2, and VCO2 were still above preinfusion levels but the RQ had decreased to 0.98 because of a decrease in VCO2. Frequency had increased from 19 +/- 4.8 breaths/min preinfusion to 22 +/- 4.7 after 4.5 hours. After 4.5 hours, VT was still above preinfusion levels while pH and PaCO2 had decreased below them. The latter was associated with an increase in serum lactate. At no time was a decrease in tidal volume observed. Therefore, the infusion of these hormones does not simulate all the alterations observed during trauma and sepsis.
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PMID:The metabolic and ventilatory response to the infusion of stress hormones. 308 92

The metabolism of the sea raven, Hemitripterus americanus, hepatocyte preparation was studied, emphasizing the roles of insulin and glucagon on carbohydrate status. Sea raven hepatocyte glycogen was depleted throughout the preincubation and 2-hr incubation period in the presence of either glucose or serine. Bovine glucagon stimulated glycogen loss and increased glucose levels and serine flux to glucose. Porcine insulin prevented glycogen depletion at least over 1.5 hr of incubation, but did not affect glucose levels in the hepatocytes. It also significantly increased serine flux to glucose, glycogen, and protein, and alanine flux to glucose, CO2, and protein. Teleost insulin did not alter the pattern of hepatic glycogen depletion, while it did increase glucose levels and serine flux to glucose, glycogen, and lipids, and alanine flux to CO2 and glucose. Both glucagon and porcine insulin increased glucose flux to glycogen, but neither altered glucose conversion to CO2, lactate, or protein. The teleost insulin had no effect on glucose conversion to any product tested. Teleost insulin had an additive effect on the glucagon-induced increases in total glucose production and gluconeogenesis from serine, while glucagon offset the insulin stimulation of serine flux to glycogen and CO2. The results demonstrate that glucagon functions to increase glucose production from gluconeogenic precursors and glycogen in sea raven hepatocytes, while insulin demonstrates anabolic effects through gluconeogenic precursors. It is suggested that insulin functions in sea raven hepatocytes to increase glycogen stores through increased amino acid utilization and/or to increase glucose production for transport to, and storage in, glucose-utilizing tissues (e.g., muscle). An antagonism between insulin and glucagon on the glycolytic/gluconeogenic pathways as is found in mammalian livers is not as clear in sea raven hepatocytes. These findings are consistent with the carnivorous diet of the sea raven and a preferentially gluconeogenic role for the liver of this species.
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PMID:Metabolism in sea raven (Hemitripterus americanus) hepatocytes: the effects of insulin and glucagon. 310 67

Glucagon was injected directly into the ventromedial hypothalamic nuclei (VMH) of rabbits, and changes in hepatic acetate metabolism were studied. The injection of 3 ng glucagon into the VMH of intact rabbits increased the rates of 14C transfer from 14C-1-acetate into CO2, glucose and ketone bodies but decreased those into cholesterol ester, triglyceride, free cholesterol, free fatty acids and phospholipids. However, after glucagon injection into the VMH of rabbits with VMH lesions and the parietal cortex of intact rabbits, hepatic acetate metabolism did not differ from that of the control rabbits, which received saline injection into the same brain regions. These observations support the hypothesis that the VMH are parts of a glucagon-sensitive brain regulator system in the hepatic acetate metabolism.
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PMID:Influence of microinjection of glucagon into ventromedial hypothalamus on acetate metabolism in liver slices of rabbit. 310 27

1. Whole-body, hind-limb and uterine tissue metabolism of glucose was studied using a combination of isotopic and arterio-venous difference techniques in shorn and unshorn pregnant sheep over the final 4 weeks of pregnancy. This was combined with the measurement of the concentrations of oxygen and carbon dioxide in arterial blood and plasma concentrations of lactate, acetate, non-esterified fatty acids, 3-hydroxybutyrate, glycerol, growth hormone (GH), insulin, glucagon, cortisol, thyroxine and 3,5,3'-triiodothyronine (T3). 2. Glucose entry rate was 28% higher in shorn ewes compared with unshorn controls, even though there was no difference in the arterial plasma concentration of glucose. This effect may have been caused by a decrease in the molar rate, insulin: glucagon (I:G), which was 40% lower in shorn ewes as a result of a significant decrease in the plasma concentration of insulin. There was no difference in the plasma concentration of cortisol or GH. 3. Blood flow across the hind-limb or uterine tissues was not significantly different between shorn and unshorn groups, neither were the net glucose uptake, glucose oxidation rate or contribution of glucose to O2 consumption across these tissues. 4. Insulin-tolerance tests performed on a separate group of shorn and unshorn ewes showed an increased sensitivity to the hypoglycaemic effects of insulin in the shorn group. 5. There was no significant difference between shorn and unshorn animals in the contribution of glucose to CO2 output or in the proportion of glucose entry rate oxidized. CO2 entry rate was 18% higher in shorn ewes compared with unshorn controls which resulted in a 26% higher estimated value for heat production. There was a 47% increase in glucose oxidation rate in shorn ewes but there was no significant difference in the proportion of total heat production which was derived from glucose. The arterial concentrations of O2 and CO2 were significantly higher in shorn ewes, which may be an indication of the higher metabolic rate in these animals. This effect may be mediated via a significant rise in plasma T3 concentration in the shorn group. 6. It is concluded that as a result of long-term cold exposure there is a significant increase in whole-body glucose entry and oxidation rates in the shorn pregnant ewe. The increase in insulin sensitivity at the same time as a decrease in plasma insulin concentration may represent a mechanism to ensure continued glucose supply to insulin-sensitive tissues while the concomitant decrease in plasma I:G stimulates hepatic gluconeogenesis.
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PMID:Glucose metabolism in shorn and unshorn pregnant sheep. 314 99


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