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 present study addressed the effects of carbohydrate consumption during endurance exercise on performance, energy turnover, and metabolism. Well-trained endurance runners consumed a beverage with (cho[+]) or without (cho[-]) carbohydrates during a long-distance run (46.6 km). The respiratory quotient (RQ), plasma levels of carbohydrate and fat metabolites, and of hormones (insulin, glucagon) were measured before, several times during, and after the run. The mean running speed for the entire distance was 13.6 and 13.4 km/h with the cho[+] and cho[-] beverage, respectively. The decrease in speed that was observed towards the end of the run was somewhat more pronounced with consumption of the cho[-] beverage. The RQ decreased during the run almost linearly. This decrease was independent of the consumed beverage. The changes in plasma levels of lactate, free fatty acids (FFA), glycerol, D-3-hydroxybutyrate (DHB), glucagon and insulin that occurred during the run were not affected by intake of the cho[+] beverage. However, intake of the cho[+] beverage prevented the decrease in plasma glucose observed towards the end of the run under control conditions, and eliminated the steep postexercise increase in plasma DHB. The intake of the cho[+] beverage also caused a rapid decrease in plasma levels of FFA and glucagon after the run, and slightly increased plasma insulin. The results demonstrate that ingestion of a carbohydrate-containing beverage during a long-distance run affects metabolism only during the final phase of the run and during the subsequent recovery period. Moreover, carbohydrate consumption improves performance only during the final phase of a long-distance run.
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PMID:[Effect of carbohydrate intake during a long distance run on work capacity and metabolism]. 158 83

Continuous exposure of cells to a hormonal stimulus results in attenuation of the hormone's effects on the cell; a process known as desensitization. The present study was undertaken to determine whether glucagon (GLU) induces desensitization of its lipolytic effect in adipocytes isolated from the abdominal fat of market-age broilers. Preincubation of adipocytes with 10 to 100 ng/mL of porcine GLU (pGLU) or chicken GLU (cGLU) for 24 h reduced (P less than .05) GLU-stimulated lipolysis. However, pGLU decreased (P less than .05) lipolysis to a greater extent than cGLU. Maximal lipolysis was reduced 70% by pGLU and 55% by cGLU. Chicken GLU also exhibited lower biological potency for acutely stimulating lipolysis from control and cGLU-treated adipocytes. Glycerol release from control adipocytes incubated for 1 h with .3 ng/mL of cGLU or pGLU was 26 and 42 nmol/h per 3% cells, respectively. The GLU-induced decrease in lipolysis occurred rapidly and was partially reversible. The results of the present study indicated that GLU induced desensitization of its lipolytic effect in broiler adipocytes.
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PMID:Glucagon-induced desensitization of broiler adipocyte lipolysis. 161 41

Euglycemic-hyperinsulinemic clamps were performed on six healthy untrained individuals to determine whether exercise that induces muscle damage also results in insulin resistance. Clamps were performed 48 h after bouts of predominantly 1) eccentric exercise [30 min, downhill running, -17% grade, 60 +/- 2% maximal O2 consumption (VO2max)], 2) concentric exercise (30 min, cycle ergometry, 60 +/- 2% VO2max), or 3) without prior exercise. During the clamps, euglycemia was maintained at 90 mg/dl while insulin was infused at 30 mU.m-2.min-1 for 120 min. Hepatic glucose output (HGO) was determined using [6,6-2H]glucose. Eccentric exercise caused marked muscle soreness and significantly elevated creatine kinase levels (273 +/- 73, 92 +/- 27, 87 +/- 25 IU/l for the eccentric, concentric, and control conditions, respectively) 48 h after exercise. Insulin-mediated glucose disposal rate was significantly impaired (P less than 0.05) during the clamp performed after eccentric exercise (3.47 +/- 0.51 mg.kg-1.min-1) compared with the clamps performed after concentric exercise (5.55 +/- 0.94 mg.kg-1.min-1) or control conditions (5.48 +/- 1.0 mg.kg-1.min-1). HGO was not significantly different among conditions (0.77 +/- 0.26, 0.65 +/- 0.27, and 0.66 +/- 0.64 mg.kg-1.min-1 for the eccentric, concentric, and control clamps, respectively). The insulin resistance observed after eccentric exercise could not be attributed to altered plasma cortisol, glucagon, or catecholamine concentrations. Likewise, no differences were observed in serum free fatty acids, glycerol, lactate, beta-hydroxybutyrate, or alanine. These results show that exercise that results in muscle damage, as reflected in muscle soreness and enzyme leakage, is followed by a period of insulin resistance.
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PMID:Eccentric exercise induces transient insulin resistance in healthy individuals. 162 73

This study was initiated to elucidate the mechanisms behind valproate-induced weight gain. Eight patients with epilepsy were studied with identical examination programs before and during the end of the first month of treatment with sodium valproate (VPA). The measurements included registration of food intake, indirect calorimetry, and determination of pancreatic and thyroid hormones, catecholamines, albumin, electrolytes, glycerol, and free fatty acids. Measurements were performed both at the basal condition and during a 3-hour oral glucose tolerance test (OGTT). After the start of VPA treatment, the mean levels during the OGTT of plasma glucose and catecholamines were significantly decreased by 7% and 25%, respectively (P less than .05). The mean ratio of insulin to glucagon decreased by 37% (P less than .01). During the glucose load, the decreases in free fatty acids were less pronounced after the start of VPA treatment, whereas the mean levels of glycerol were found to be unchanged. We detected no differences between the two periods with regard to total energy intake or macronutrient selection, energy expenditure, or thyroid hormones. As VPA is known to affect the concentration of carnitine in humans, it is hypothesized that a possible VPA-induced deficiency of the beta-oxidation of fatty acids is important for the development of obesity in epileptic patients in long-term treatment with VPA, but changes in catecholamines or other hormones might also be of importance.
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PMID:Metabolic changes during treatment with valproate in humans: implication for untoward weight gain. 164 Aug 53

Cultured rat hepatocytes were preincubated with glucagon or a cyclic AMP analogue for up to 24 h and lipid synthesis and secretion were determined during the next 2 h. Glucagon or cyclic AMP did not change the incorporation of choline or glycerol into phosphatidylcholine, or choline into sphingomyelin, in the cells after 0-12 h of preincubation. After 12 h these incorporations were increased. Incorporations into hepatic lysophosphatidylcholine were decreased after preincubation with glucagon or cyclic AMP for 0-12 h, but by 24 h they increased. There was no change in the lysophosphatidylcholine in the medium after preincubation with glucagon or cyclic AMP for up to 6 h, but increases occurred after preincubation from 12 to 24 h. The secretion of triacylglycerol was decreased after preincubation for 0-1 h, but it returned to control values after 4 h. After preincubation for 18-24 h the incorporation of glycerol into secreted triacylglycerol was increased. The results are discussed in relation to the control of lipid metabolism in starvation and diabetes.
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PMID:Biphasic effects of glucagon and cyclic AMP on the synthesis and secretion of lipids by rat hepatocytes. 165 86

We investigated the tubular action of endothelin in rat nephron segments. The effects of endothelin on arginine vasopressin (AVP)-, parathyroid hormone-, glucagon-, calcitonin-, and isoproterenol-dependent cAMP accumulation were studied. The following nephron segments were microdissected: glomerulus (Gl), proximal convoluted tubule (PCT), cortical and medullary thick ascending limbs of Henle's loop (cTAL and mTAL, respectively), cortical collecting duct (CCD), outer medullary collecting duct (OMCD), and inner medullary collecting duct (IMCD). Endothelin dose dependently (10(-8)-10(-10)M) inhibited AVP-dependent cAMP accumulation in CCD, OMCD, and IMCD. This effect was independent of the presence or absence of phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, Ca channel blocker nicardipine, or indomethacin, but was abolished in the presence of protein kinase C inhibitor H-7. Protein kinase C stimulator dioctanoyl glycerol mimicked the effect of endothelin. On the other hand, endothelin had no inhibitory effect on AVP-dependent cAMP accumulation in cTAL or mTAL, parathyroid hormone-dependent cAMP accumulation in Gl and PCT, or glucagon-, calcitonin-, and isoprotereol-dependent cAMP accumulation in OMCD. We conclude that endothelin specifically inhibits AVP-dependent cAMP accumulation in CCD, OMCD, and IMCD through activating protein kinase C. This effect possibly has a role in maintaining urine volume to counteract the decrease in GFR caused by endothelin itself.
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PMID:Effects of endothelin on peptide-dependent cyclic adenosine monophosphate accumulation along the nephron segments of the rat. 169 79

This study was designed to find out whether rest intervals and prevention of dehydration during prolonged exercise inhibit a drift in metabolic rate, body temperature and hormonal response typically occurring during continuous work. For this purpose in ten healthy men the heart rate (fc), rectal temperature (Tre), oxygen uptake (VO2), as well as blood metabolite and some hormone concentrations were measured during 2-h exercise at approximately 50% maximal oxygen uptake split into four equal parts by 30-min rest intervals during which body water losses were replaced. During each 30-min exercise period there was a rapid change in Tre and fc superimposed on which, these values increased progressively in consecutive exercise periods (slow drift). The VO2 showed similar changes but there were no significant differences in the respiratory exchange ratio, pulmonary ventilation, mechanical efficiency and plasma osmolality between successive periods of exercise. Blood glucose, insulin and C-peptide concentrations decreased in consecutive exercise periods, whereas plasma free fatty acid, glycerol, catecholamine, growth hormone and glucagon concentrations increased. Blood lactate concentrations did not show any regular drift and the plasma cortisol concentration decreased during the first two exercise periods and then increased. In conclusion, in spite of the relatively long rest intervals between the periods of prolonged exercise and the prevention of dehydration several physiological and hormonal variables showed a distinct drift with time. It is suggested that the slow drift in metabolic rate could have been attributable in the main to the increased concentrations of heat liberating hormones.
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PMID:Metabolic, body temperature and hormonal responses to repeated periods of prolonged cycle-ergometer exercise in men. 173 7

The present study was undertaken to evaluate the metabolic and hormonal responses to physiologic elevations of plasma beta-endorphin concentrations in both normal-weight and obese healthy subjects. The infusion of synthetic human beta-endorphin (4.5 ng/kg/min) produced the following: (1) in normal-weight subjects, no significant change of plasma glucose and pancreatic hormones (insulin, C-peptide, and glucagon), a significant plasma free fatty acids (FFA) increase, and a suppression of glycerol plasma levels; (2) in obese subjects, significant increases of glucose, insulin, C-peptide, and glucagon, a progressive decline of circulating FFA, and no change in glycerol plasma levels. In obese subjects, the intravenous administration of naloxone, given as a bolus (5 mg injected in 5 minutes) before the start of beta-endorphin infusion, reduced the plasma glucose response to the opioid by approximately half, annulled the pancreatic hormonal responses, and also reduced the FFA, but not glycerol, response. In normal-weight subjects, naloxone pretreatment did not induce any change of the flat glucose and hormonal responses to beta-endorphin, but reversed its effects on circulating FFA and glycerol. These data suggest that physiological elevations of plasma beta-endorphin concentrations produce metabolic and hormonal effects in obese subjects significantly different from those occurring in normal-weight subjects; these effects are partially naloxone-sensitive, suggesting the mediation of endogenous opioid receptors.
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PMID:Physiological elevations of plasma beta-endorphin alter glucose metabolism in obese, but not normal-weight, subjects. 173 41

This study was designed to investigate the effect of short-term, submaximal training on changes in blood substrates, metabolites, and hormonal concentrations during prolonged exercise at the same power output. Cycle training was performed daily by eight male subjects (VO2max = 53.0 +/- 2.0 mL.kg-1.min-1, mean +/- SE) for 10-12 days with each exercise session lasting for 2 h at an average intensity of 59% of VO2max. This training protocol resulted in reductions (p less than 0.05) in blood lactate concentration (mM) at 15 min (2.96 +/- 0.46 vs. 1.73 +/- 0.23), 30 min (2.92 +/- 0.46 vs. 1.70 +/- 0.22), 60 min (2.96 +/- 0.53 vs. 1.72 +/- 0.29), and 90 min (2.58 +/- 1.3 vs. 1.62 +/- 0.23) of exercise. The reduction in blood lactate was also accompanied by lower (p less than 0.05) concentrations of both ammonia and uric acid. Similarly, following training lower concentrations (p less than 0.05) were observed for blood beta-hydroxybutyrate (60 and 90 min) and serum free fatty acids (90 min). Blood glucose (15 and 30 min) and blood glycerol (30 and 60 min) were higher (p less than 0.05) following training, whereas blood alanine and pyruvate were unaffected. For the hormones insulin, glucagon, epinephrine, and norepinephrine, only epinephrine and norepinephrine were altered with training. For both of the catecholamines, the exercise-induced increase was blunted (p less than 0.05) at both 60 and 90 min. As indicated by the changes in blood lactate, ammonia, and uric acid, a depression in glycolysis and IMP formation is suggested as an early adaptive response to prolonged submaximal exercise training.
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PMID:Early adaptations in blood substrates, metabolites, and hormones to prolonged exercise training in man. 178 5

The aim of this study was to establish the role of nerves to the liver in the disposal of an enteral glucose load. Dogs underwent a laparotomy during which the nerves to the liver were either left intact (C; n = 10) or removed (DN; n = 10). Absence of measurable liver norepinephrine was used to indicate completeness of denervation. Four weeks following surgery, 18-h fasted conscious dogs were given a glucose load (0.7 g/kg body weight) by gavage, and arterial blood samples were drawn over a 180-min period. The glucose and insulin excursions from baseline (incremental area) were 29% and 22% greater (P greater than 0.05) in DN than in C, respectively. Resting blood lactate levels were similar between groups, but they increased significantly more (P less than 0.05) following the administration of the glucose load in DN (peak change from resting level was 376 +/- 90 mumol/L in C and 728 +/- 81 mumol/L in DN). No significant differences between groups in glucagon, glycerol or alanine concentration were evident either prior to or following glucose administration. These data demonstrate that hepatic nerves can influence the substrate and hormone environment following an enteral glucose load.
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PMID:Hepatic denervation alters the disposition of an enteral glucose load in conscious dogs. 186 Nov 74


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