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)

Changes in perfusate Ca2+ (measured with a Ca(2+)-selective electrode) and changes in bile calcium (measured by atomic absorption spectroscopy) were continuously and simultaneously monitored after infusion of (a) vasopressin, (b) glucagon and (c) both vasopressin and glucagon together to the perfused rat liver. Also monitored were perfusate glucose and oxygen concentrations and bile flow. Vasopressin induces a sharp, transient, pulse of increased bile flow and increased bile calcium within 1 min of infusion, concomitant with rapid changes in perfusate Ca2+ fluxes, glucose output and oxygen uptake. This is immediately followed by a decrease in both bile flow and bile calcium for as long as the hormone is administered. Changes induced by glucagon are a relatively slow onset of perfusate Ca2+ efflux and oxygen uptake, but rapid glucose output, and a small but significant and transient decrease in bile flow and bile calcium which, despite the continued infusion of the hormone, spontaneously and rapidly returns to normality. However, the greatest responses are observed after co-administration of both hormones. Coincident with the augmented perfusate Ca2+ fluxes (influx) seen in earlier work, there occurs within 1 min of vasopressin infusion a sharp increase in bile secretion and bile calcium greater in magnitude than that produced by vasopressin alone. Immediately thereafter bile secretion and bile calcium decline below basal values and remain there for as long as the hormones are administered. Glucagon and vasopressin therefore each have opposing effects on bile flow and bile calcium. However, the action of vasopressin is enhanced by the prior administration of glucagon. The data thus reveal features about the actions of glucagon and Ca(2+)-mobilizing hormones on bile flow and bile calcium not previously recorded and provide a novel framework around which the whole issue of hepato-biliary Ca2+ homoeostasis can be assessed in normal and diseased liver.
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PMID:Concomitant stimulation by vasopressin of biliary and perfusate calcium fluxes in the perfused rat liver. 173 88

The interrelationship between glycogen biosynthesis and do novo glucose formation in rats was studied by determining the oxaloacetic acid, ATP, and glycogen levels in the tissues of healthy starved rats and during the growth of transplantable hepatomas with different rates of growth. From the results obtained it was proposed that glycogen biosynthesis and de novo glucose formation are mutually enhanced and coupled processes. The validity of this conclusion was confirmed by in vitro model experiments involving the use of isolated-liver perfusion. Results of a multiple regression analysis indicated that the efficiency of gluconeogenesis and glycogen deposition is determined by the supply of oxygen to the liver, by the oxaloacetic acid content of this organ, and also by the degree of reduction of the glucose precursor. It was also shown that the ability of glucocorticoids and glucagon to enhance gluconeogenesis is dependent on the supply of oxygen to the liver. From the results of this in vivo and in vitro comparative study it is concluded that deposition of glycogen in the liver and possibly also in the brain is determined by the efficiency of gluconeogenesis.
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PMID:Intracellular factors determining the deposition of glycogen. The role of gluconeogenesis. 175 56

Simultaneous variations of oxygen consumption, and plasma insulin and norepinephrine were measured during the postprandial cephalic and gastrointestinal phases of feeding in six human subjects following the ingestion of various nutrients. On alternative days the subjects were given foods (1280 kjoules) either rich in carbohydrates (sugar pie) or in proteins (fish). Both nutrients produced an initial (0-40 min) enhanced thermogenesis and an early (2 min) cephalic insulin release. During that period, elevations of plasma norepinephrine were also observed with pie feeding at 10 and 30 min and at 10 min with fish. Palatability ratings indicated that both food items were equally tasting. During the gastrointestinal phase (40 to 120 min) the variations of these same parameters including glucagon seem to be explained by the content in carbohydrates and proteins in the food rather than by its palatability. Indeed during that period the protein meal was more thermogenic and the carbohydrate meal induced the expected insulin secretion. These results suggest that the palatability of the food is responsible for the early cephalic increase in postprandial thermogenesis, and for the insulin and norepinephrine release. During the subsequent gastrointestinal phase the increased thermogenesis is related to the composition of the food which exerts its action by the biochemical processes involved in the disposal of the absorbed nutrients.
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PMID:Thermogenic and hormonal responses to palatable protein and carbohydrate rich food. 177 19

Our experimental study has proved, that the increase in the intestinal and splanchnic metabolism is associated with raised blood flow. However, it has been found that so called primary increase of the blood flow by the administration of vasodilatators is not associated with raised metabolism, i.e. no increase in the oxygen uptake has been noted. Injection of Glucagon into the superior mesenteric artery raised both the splanchnic (portal vein) and the intestinal (superior mesenteric artery) blood flow. However, while the intestinal oxygen consumption increases along with the blood flow, when the blood flow to the whole splanchnic area has risen the oxygen consumption has not increased moreover it has decreased. This means, that while the Glucagon quickens the metabolism of the small bowel, that in the other abdominal organs has dropped. This means that while there is not any difference in the vascular effect of the intestinal and total splanchnic area, the metabolic effect shows a disparity, this can be regarded as an evidence, that the alterations in the splanchnic metabolism are not primarily determined by haemodynamic changes. The blood flow is adjusted to the oxygen demand and the physiological changes in the blood flow protect against cellular hypoxia under various circumstances.
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PMID:The relationship between splanchnic oxygen consumption and blood supply. 181 63

Comparatively low level of serum insulin and tissue insulin resistance are characteristic of the stage of burn hypermetabolism. In order to evaluate the effect of tolbutamide in reducing burn hypermetabolism rate, 18 adult male rabbits weighing 1.8-2.5 Kg were subjected to 30% TBSA full thickness burns and randomized into treated and control groups. In the treated group, tolbutamide (90mg/Kg/day) was introduced into the stomach from 4 hours to 10 days postburn. Animals of both group were fed with specified food (protein 15%, glucose 80%) after burn. The values of serum glucose, insulin, glucagon, oxygen expenditure and other nutritional indices were measured before burn and 1, 3, 6, 10 days postburn. Their changes were as follows: (1) Serum glucose levels of the treated group were obviously lower than those of the control group (P less than 0.01). (2) Serum insulin levels and the ratio of I/G (insulin/glucagon) of the treated group were significantly higher than those of the control group (P less than 0.01). (3) The indices of cumulative N balance, oxygen expenditure, serum albumin in the treated group were better than that in the control (P less than 0.05-0.001). It is concluded that tolbutamide can reduce burn hypermetabolism probably through the following ways: 1. stimulation of the secretion of insulin and enhancement of the effect of insulin; 2. inhibition of the secretion of glucagon; 3. improvement in tissue insulin resistance and promotion of glucose utilization of skeletal muscles.
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PMID:[Tolbutamide and burn hypermetabolism]. 203 79

In liver phosphoenolpyruvate carboxykinase (PCK) activity, protein and mRNA are localized predominantly in the periportal zone. The activation of the PCK gene by glucagon was studied in primary rat hepatocyte cultures under physiological arterial and venous oxygen tensions [16% and 8% (by vol.)]. PCK gene expression was monitored on the level of transcription, mRNA abundance and enzyme activity as well as enzyme synthesis and degradation. 1. Transcription of the PCK gene was increased by 10 nM glucagon maximally after 0.5 h; it reached nearly basal levels again after 2 h. The increase in transcription was 45% lower under 8% oxygen than under 16% oxygen. 2. PCK mRNA was maximally increased after 2 h under 16% oxygen and after 4 h under 8% oxygen; it subsequently declined to twice the basal values after 8 h. The maximal increase after 2 h was 50% lower under 8% oxygen than under 16% oxygen. 3. PCK enzyme activity was maximally increased after 4-6 h. The maximal enhancement after 4 h was 50% lower under 8% oxygen than under 16% oxygen. 4. The increase in PCK enzyme activity was due to an enhanced synthesis rate of PCK protein. The rate increased after 3 h was 35% lower under 8% oxygen than under 16% oxygen. 5. The degradation of PCK protein was equal under both oxygen tensions. The results show that in cultured rat hepatocytes the induction of PCK gene expression is modulated by physiological concentrations of oxygen. The modulation occurred at the level of gene transcription, mRNA abundance, enzyme protein synthesis and enzyme activity. The periportal to perivenous oxygen gradient could be the major factor responsible for the predominant expression of the PCK gene in the periportal zone.
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PMID:Modulation by oxygen of the glucagon-dependent activation of the phosphoenolpyruvate carboxykinase gene in rat hepatocyte cultures. 205 Jan 45

The present study was performed to determine whether alterations in fuel reserves or energy substrate utilization might explain the performance decrements that occur in bacterial infections. Male Fisher-Dunning rats were studied at 24, 48, and 72 h after inoculation with Streptococcus pneumoniae. Rats were either sedentary or subjected to a 2-h swimming session at these three time points (N = 10 in each group). A more than 60% reduction (P less than 0.01) in performance capacity was observed on day 3 of infection compared with that in noninfected controls. This infection in the rat is characterized by fever (P less than 0.01), depression of plasma zinc (P less than 0.01) and free fatty acid (FFA) levels (P less than 0.01), inhibition of the two- to threefold increase in fasting ketonemia, and a decreased (NS) insulin:glucagon ratio, indicating a catabolic state. Glycogen stores were reduced in the heart (47%), liver (43%), and skeletal muscles (39%) but not in the carcass. Superimposed exercise resulted in a further reduction but not depletion of liver, muscle, and carcass glycogen stores, a less pronounced lactic acid accumulation, and a lower oxygen debt. However, plasma FFA and ketone body levels were still maintained or even elevated, suggesting that fat is supplied as fuel during swimming exercise in this infection. Thus, results indicate that unavailability of energy substrates or lactacidosis is not limiting for performance capacity during this severe infection.
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PMID:Metabolic responses to swimming exercise in Streptococcus pneumoniae infected rats. 205 98

Significant reduction of total and coupled respiration as well as an increase of uncoupled respiration characterize the maturation of rat reticulocytes. ATP declines by 45%, whereas ADP increases by 70% and the ATP/ADP ratio decreases from 7.6 to 3.3. At the same time the oxygen-delivery capacity of red blood cells increases by 37% due to an increase of 2.3-BPG level. In the youngest reticulocytes the basic level of cAMP is 2-fold higher, whereas the maximal (-)-isoproterenol-induced accumulation of cAMP is 8-fold higher than in the fraction of most mature reticulocytes. Evidence for the presence of functionally active glucagon-receptors in reticulocytes is presented, with maturational inactivation/disappearance of R2-glucagon receptors.
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PMID:Maturation-dependent changes of the rat reticulocyte energy metabolism and hormonal responsiveness. 216 79

We investigated the kinetics of the mitochondrial respiratory chain, proton leak, and phosphorylating subsystems of liver mitochondria from mannoheptulose-treated and control rats. Mannoheptulose treatment raises glucagon and lowers insulin; it had no effect on the kinetics of the mitochondrial proton leak or phosphorylating subsystems, but the respiratory chain from succinate to oxygen was stimulated. Previous attempts to detect any stimulation of cytochrome c oxidase by glucagon are shown by flux control analysis to have used inappropriate assay conditions. To investigate the site of stimulation of the respiratory chain we measured the relationship between the thermodynamic driving force and respiration rate for the span succinate to coenzyme Q, the cytochrome bc1 complex and cytochrome c oxidase. Hormone treatment of rats altered the kinetics of electron transport from succinate to coenzyme Q in subsequently isolated mitochondria and activated succinate dehydrogenase. The kinetics of electron transport through the cytochrome bc1 complex were not affected. Effects on cytochrome c oxidase were small or nonexistent.
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PMID:Stimulation of the electron transport chain in mitochondria isolated from rats treated with mannoheptulose or glucagon. 217 25

After an overnight fast, blood samples were obtained from seven obese women (50% +/- 3% body fat) and from seven control women (25% +/- 1% body fat) before, during, and after 10 minutes of treadmill exercise at 70% of each individual's maximal oxygen uptake (VO2max). During exercise, peak plasma epinephrine (E), norepinephrine (NE), and glucagon concentrations in the control group significantly exceeded corresponding peak values in the obese group by 1.4-fold to twofold, whereas lactate responses did not differ. After 5 minutes of rest, peak plasma glucose, free fatty acid (FFA), and growth hormone (GH) concentrations in the control group also were significantly higher than in the obese women, but the plasma cortisol responses were comparable. Although plasma insulin concentrations decreased during exercise and rose to maximum values at 5-minute recovery in all individuals, levels were more than 3.5-fold higher in the obese group throughout the study. We conclude that the combination of heightened plasma insulin and diminished catecholamine and other counterregulatory hormone responses may account for subnormal plasma substrate increments that distinguish obese from non-obese women during exercise at comparable work intensities.
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PMID:Impaired plasma catecholamine response to submaximal treadmill exercise in obese women. 218 75


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