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 effects of ingesting a low dose of CHO on plasma glucose, glucoregulatory hormone responses, and performance during prolonged cycling were investigated. Nine male subjects cycled for 165 min at approximately 67% peak VO2 followed by a two-stage performance ride to exhaustion on two occasions in the laboratory. Every 20 min during exercise, subjects consumed either a flavored water placebo (P) or a dilute carbohydrate beverage (C). Blood samples were collected immediately before, every 20 min throughout, and immediately after exercise. Plasma was analyzed for glucose, lactate, free fatty acids (FFA), and various glucoregulatory hormones. VO2, RER, heart rate, perceived exertion, and exercise performance were also measured. Lactate, FFA, epinephrine, norepinephrine, ACTH, cortisol, and glucagon increased with exercise whereas glucose and insulin decreased (p < or = .05). Except for a small difference in glucose at 158 min of exercise and at exhaustion, no significant differences were found between drinks for any of the variables studied (P > or = .05). Ingestion of 13 g carbohydrate per hour is not sufficient to maintain plasma glucose, attenuate the glucoregulatory hormone response, and improve performance during prolonged moderate intensity cycling.
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PMID:Failure of low dose carbohydrate feeding to attenuate glucoregulatory hormone responses and improve endurance performance. 166 7

6-hydroxydopamine (6-OHDA) was utilised for the study of the sympathetic nervous system in the resting rats and rats submitted to prolonged exercise. In order to reduce the acute physiological stress associated with an injection of 6-OHDA, beta-1 and alpha-1 adrenoceptors were blocked before the treatment leading to sympathectomy. Sympathectomised rats were divided in two groups: one sacrificed at rest, 24 hours after the treatment. The other group was sacrificed after a treadmill exercise to exhaustion. Running time to exhaustion was 36.0 +/- 4.5 min (mean +/- S.E.M.). This group ran significantly less than a control group brought to exhaustion in 73.7 +/- 10.0 min of exercise (P < 0.05). In order to make appropriate comparisons, another control group was run for 36 min. Some differences were observed between corresponding control and sympathectomized groups. At rest: 1) a lower plasma level of insulin, and 2) a higher plasma free fatty acid concentration were observed in sympathectomized rats. After 36 min of exercise: 1) a lower plasma concentration of norepinephrine, 2) no decrease of the plasma level of insulin, 3) no increase in the plasma glucagon concentration, and 4) a higher plasma glucose level were observed in sympathectomised rats when compared to control rats running for the same time. The lower plasma norepinephrine concentration in exercised sympathectomised rats suggests a lower sympathetic nervous activity in these animals than in control rats. The absence of a decrease of plasma insulin concentration and of an increase in glucagon can be attributed to this lower sympathetic activity in sympathectomised rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:6-OHDA sympathectomy and exercise performance in the rat. 170 82

Glucose turnover and its regulation were studied during and after two identical bouts of intense exhaustive exercise separated by 1 h to define differences in response. Six lean young postabsorptive male subjects exercised at approximately 100% maximal O2 uptake (3.7 +/- 0.3 l/min) for 13.0 +/- 0.7 min for the first (EX1) and 13.2 +/- 0.8 min for the second (EX2) bout. Plasma glucose increased during EX1 and peaked at 7.0 +/- 0.6 mmol/l in early recovery but to 5.8 +/- 0.5 mmol/l (P less than 0.05) after EX2, and both the hyperglycemic and the hyperinsulinemic responses were less after EX2 (P less than 0.015, analysis of variance). The hyperglycemia was due to lesser increments in glucose utilization (Rd) (3-fold resting) than glucose production (Ra) (7-fold) toward exhaustion and for 7 min of recovery. The rise in Rd was more rapid (P less than 0.05) and metabolic clearance rate was greater during (P = 0.015) and from 9 to 60 min after EX2, and Ra also remained higher during recovery (P less than 0.05). Marked and similar increments in plasma norepinephrine (18-fold) and epinephrine (14-fold) occurred with both bouts. Plasma glucagon increments were small and not different. Therefore, 1) more circulating glucose was used with EX2, 2) greater metabolic clearance rate during and after EX2 suggests local muscle adaptations due to EX1, and 3) significant correlations (P less than 0.002) between plasma norepinephrine and Ra (r = 0.82) and Ra - Rd (r = 0.52) and between epinephrine and Ra (r = 0.71) and Ra - Rd (r = 0.48) suggest a major regulatory role for the catecholamine responses.
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PMID:Glucoregulatory and hormonal responses to repeated bouts of intense exercise in normal male subjects. 175 30

The influence of 10 mg carteolol/day on the serum concentrations of insulin, C-peptide, glucagon, free fatty acids, adrenaline, noradrenaline, blood glucose, blood lactate levels, on heart rate and systolic blood pressure was investigated during different workloads on a bicycle ergometer in a placebo-controlled randomised double-blind study involving twelve male volunteers. The subjects performed standardized increasing exercises until subjective exhaustion as well as three 40-minute endurance exercises of varying intensity, corresponding to a lactate concentration of 1.0 to 2.0 mmol/l, 2.5 to 3.5 mmol/l and more than 3.5 mmol/l in the region of the anaerobic threshold, each exercise being followed by one rest day. The most important findings are: --the ISA of carteolol is of significance for the influence on the heart rate at rest but plays a minor role with respect to the degree of reduction in the heart rate and blood pressure under exercise; --carteolol exerts a minor influence on the metabolic parameters investigated in this study. This can be partly ascribed to the pronounced ISA of carteolol. In the case of endurance exercises, which lead to blood lactate concentrations of more than 3 mmol/l, the blood glucose levels showed a tendency to decrease. However, this was not statistically significant.
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PMID:An examination of the hemodynamic and metabolic effects of carteolol during different workloads on a bicycle ergometer. 179 96

The liver, through the afferent ways of the vagus hepatic nerve, may influence metabolic adaptations during exercise. This study assesses the functional significance of this hepatic innervation by determining the effect of a selective hepatic vagotomy (HV) on running endurance time during submaximal activity in rats subjected to an overnight 50% food restriction. The time to exhaustion was similar for the groups of HV and sham-operated (SHM) rats [66 +/- 15 vs. 64 +/- 21 (SD) min]. The HV group was associated with higher resting levels (P less than 0.05) of hepatic glycogen and plasma glucose. No significant differences were observed between HV and SHM rats at rest and after exercise for muscle glycogen, free fatty acids, insulin, glucagon, and lactate concentrations. These data indicate that if hepatic glucoreceptors do exist and contribute to the metabolic regulation of exercise, their functional significance is secondary to more important regulatory mechanisms.
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PMID:Effects of selective hepatic vagotomy on running endurance in rats. 207 16

This study compared the effects of glucose feeding and water on endurance performance, glycogen utilization, and endocrine responses to exhaustive running in rats. Forty-eight trained rats ran at approximately 70% peak O2 consumption (VO2) while receiving, via gavage, 1 ml of an 18% glucose solution or water every 30 min. Glucose- (GF) and water-fed rats (WF) were pair matched and killed at rest, at 25 or 50% of their previously determined run time to exhaustion, or at exhaustion. Run times to exhaustion were 4.6 +/- 1.0 and 3.0 +/- 0.9 h in GF and WF rats, respectively. In WF rats, plasma glucose declined continuously from a resting value of 7.4 +/- 0.5 to 1.8 +/- 0.5 mM at exhaustion and was lower than in GF rats at all exercise time points. In GF rats, glucose was maintained at 7.4 +/- 0.5 mM for 3 h before dropping to 3.9 +/- 0.6 mM at exhaustion. In both groups, liver and muscle glycogen decreased dramatically during the 1st h and changed only slightly thereafter. During the 3rd h, glycogen levels were maintained in GF rats but continued to decrease in WF rats (P less than 0.05). Insulin decreased during exercise and was not significantly different between groups. Glucagon, epinephrine, norepinephrine, and corticosterone increased to a greater extent in WF than in GF rats during the first 3 h of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose feedings and exercise in rats: glycogen use, hormone responses, and performance. 224 86

Exogenous fructose 1,6-diphosphate (FDP), a glycolytic intermediate, has recently been demonstrated to accelerate ATP production, prevent glycogen breakdown, stimulate glycogen synthesis, and synthesize free fatty acids in animals and humans. To assess the effects of FDP on the hormonal and metabolic response to exercise, ten trained males (34 +/- 7 yr) underwent 1 h of continuous exercise at 70% VO2max followed by 20 W.min-1 increments to exhaustion. Two hundred fifty mg.kg-1 body weight FDP or placebo was infused in randomized, double-blind, crossover fashion. No differences were observed in heart rate, blood pressure, gas exchange data, perceived effort, or glucose, insulin, free fatty acid, lactate, beta-hydroxybutyrate, glycerol, and glucagon concentration at rest, during exercise, or upon exhaustion. In contrast to the previously reported bioenergetic effects of FDP under conditions in which glycolysis is impeded (acidosis, hypoxia, and ischemia), FDP did not affect the gas exchange, hormonal, or substrate response to moderately high intensity exercise in healthy normals.
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PMID:Effect of fructose 1,6-diphosphate infusion on the hormonal response to exercise. 240 38

The concept of islet exhaustion maintains that exposure of pancreatic islets to hyperglycemia and other stresses leads to islet dysfunction and irreparable damage. The process of pancreatic transplantation places many stresses on islets (e.g., counter-regulatory hormones, steroids, cyclosporine toxicity). As practiced by some centers, it may be important to administer exogenous insulin in the postoperative period to provide islet rest. Using a porcine pancreas transplant model that simulates clinical transplantation, we studied 2 groups: 1 group (n = 8) received constant insulin infusion for 7 days after transplantation; the control group (n = 5) received vehicle only. The islets in the insulin infusion group were rested as evidenced by a significantly decreased mean C-peptide level (0.27 +/- 0.04 ng/ml) as compared to the control group (0.66 +/- 0.08 ng/ml) (P less than 0.05). After insulin infusion was discontinued, intravenous glucose tolerance testing found insulin, C-peptide and glucagon responses were not different between groups. Glucose clearance was also comparable; K values were -1.79 and -1.60 in the insulin infusion and control groups, respectively. In conclusion, islet rest by insulin infusion for 7 postoperative days did not improve subsequent pancreas transplant endocrine function.
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PMID:No improvement of pancreas transplant endocrine function by exogenous insulin infusion (islet rest) in the postoperative period. 250 20

Exercise is associated with a marked increase in glucose uptake by muscle, which is initially supported by breakdown of hepatic glycogen and subsequently by increased gluconeogenesis. If hepatic glucose production is inadequate, hypoglycemia results. During exercise there is decreased plasma insulin and increased catecholamines, glucagon, cortisol, and growth hormone, which contribute to but are not essential for the increased hepatic output of glucose. Although insulin concentrations fall, insulin sensitivity is increased. However, the augmented glucose uptake by muscle is due to other factors. The symptoms of exhaustion during exercise are not due to hypoglycemia, and prevention of hypoglycemia may not prolong the time of exercise to exhaustion. During severe caloric restriction, hepatic glucose production decreases and free fatty acids and ketone bodies become important sources of calories. Although under these circumstances hepatic gluconeogenesis is usually sufficient to prevent hypoglycemia, with very severe caloric restriction hypoglycemia can result. With starvation, insulin concentrations fall while growth hormone and glucagon increase. Frequently the usual symptoms of hypoglycemia are absent in individuals with hypoglycemia from severe caloric restriction. Hypoglycemia from severe caloric restriction has not been totally restricted to underdeveloped areas of the world. In such patients no endocrine abnormalities have been found, and hypoglycemia has persisted despite administration of large amounts of carbohydrate. Pregnancy and lactation could predispose to hypoglycemia in the face of inadequate caloric intake.
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PMID:Exercise and deficient carbohydrate storage and intake as causes of hypoglycemia. 264 24

Thirteen highly trained subjects were studied concerning the effect of consuming a normal carbohydrate-rich diet (N) on energy exchange, substrate metabolism, and performance. Six of these subjects performed the same protocol receiving N supplemented with a high-maltodextrin, low-fructose beverage (Mf). The studies were performed in random order. The subjects performed 2 days of sustained exhausting cycling, preceded and followed by a standardized resting day, in a respiration chamber, allowing continuous gas analysis, weighed food and fluid intake procedures, collection of excretes, and drawing of blood samples at 7:00 AM, 12:00 AM (halfway exercise) and 3:00 PM at exhaustion. Muscle biopsies were taken prior to, 45 min after, and 24 h after exercise (energy expenditure 25.2-26.6 MJ.day-1). The results showed that while consuming a normal diet, the cyclists developed a negative energy balance (-9 MJ.day-1) and regulated their hormone levels in such a way that fat oxidation and protein breakdown were increased and CHO oxidation became depressed. When supplemented with Mf, the subjects showed increased blood glucose, insulin and decreased glucagon levels. Fat metabolism was significantly depressed as indicated by the levels of blood fatty acids, glycerol, and ketones. A significant glycogen sparing, as well as supercompensation within 24 h of recovery, was observed after Mf supplementation. The normal CHO-rich diet, available ad libitum, was insufficient to fully restore glycogen within 24 h. The changes in substrate availability and glycogen depletion were accompanied by a significant performance improvement, 126% when cycling a final 90% Wmax bout, when supplemented with Mf compared with N.
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PMID:Metabolic changes induced by sustained exhaustive cycling and diet manipulation. 266 43


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