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)

Reduced O2 availability, as might occur under some physiological and pathological conditions, stimulates insulin and glucagon release and increases glucose fluxes and muscle carbohydrate metabolism. The aim of this study was to determine the role of reduced PO2, independent of changes in glucagon and insulin. In six dogs, in paired studies separated by 2 wk, glucagon and insulin levels were fixed throughout by infusion of somatostatin with basal intraportal glucagon and insulin replacement. A control period was followed by 90 min of breathing 21% (NO) or 8% (LO) O2. Isotopic and arteriovenous methods were used to assess carbohydrate metabolism. Measured variables were constant over time in NO. Arterial PO2 (Pao2) was approximately 100 mmHg in NO and approximately 30 mmHg in LO, resulting in a 50% fall in O2 content. Insulin, glucagon, and catecholamine levels were similar in NO and LO. Cortisol was significantly increased in LO. Arterial glucose was unchanged in both groups. In the last 45 min of the experimental period in LO, 1) glucose production (14 +/- 1 to 18 +/- 1 mumol.kg-1.min-1), glucose disappearance (15 +/- 1 to 17 +/- 1 mumol.kg-1.min-1), and net hepatic glucose output (11 +/- 1 to 15 +/- 1 mumol.kg-1.min-1) rose, 2) limb pyruvate oxidation (11 +/- 2 to 24 +/- 5 mumol/min) and estimated glycogenolysis (9 +/- 3 to 42 +/- 9 mumol/min) increased, 3) percentages of CO2 from limb pyruvate and glucose increased, and percentage of lactate from blood glucose decreased, and 4) arterial blood lactate was approximately 100% more, although net limb and hepatic lactate balances were unaltered, which suggests that neither liver nor muscle is the source of increased blood lactate. Comparison of these results with our previous study [Zinker et al. Am. J. Physiol. 266 (Endocrinol. Metab. 29): E921-E929, 1994] shows that the response to reduced PaO2, although present, is reduced when glucagon and insulin levels are fixed at basal. The majority of stimulation of glucose production by decreased PaO2 is still present when pancreatic hormones are clamped at basal, while the response by the hindlimb tissues is greatly reduced.
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PMID:Contribution of pancreatic hormone responses to the elevation in carbohydrate metabolism with reduced PaO2. 761 94

The objective of this study was to examine if RU486, a corticosteroid antagonist, modified hepatocyte metabolism and blocked the metabolic effects of exogenously administered cortisol in rainbow trout (Oncorhynchus mykiss). The fish were given a single intraperitoneal implant of either coconut oil alone or coconut oil containing RU486 (100 mg.kg-1), cortisol (100 mg.kg-1), or a combination of RU486 and cortisol and were sampled 7 days postimplantation. The RU486 implants had no effect on plasma cortisol and glucose concentrations, hepatocyte glycogen content, and total glucose production, but increased in vitro hepatocyte glycogen breakdown. Cortisol implantation had no effect on plasma glucose concentration, hepatocyte glycogen content, glycogen breakdown, or total glucose production, while it significantly increased alanine oxidation and gluconeogenesis in rainbow trout hepatocytes. Hepatocyte responsiveness to epinephrine and glucagon stimulation of total glucose production was not modified by either RU486 or cortisol treatment, whereas the insulin response on total glucose production was decreased with cortisol. RU486 treatment modified hepatocyte glycogen metabolism and blocked the cortisol-induced increases in alanine gluconeogenesis and glycogen mobilization for endogenous use by the hepatocytes. These results indicate that cortisol enhances the metabolic potential of hepatocytes, thereby adapting the fish to cope with stress. This study provides further validation of RU486 as a tool for studying metabolic actions of cortisol in fish.
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PMID:The effects of cortisol on hepatocyte metabolism in rainbow trout: a study using the steroid analogue RU486. 784 70

In Montreal, Quebec, a randomized, double blind study was conducted in eight healthy men at Hotel-Dieu Hospital during administration of cortisol (2 mcg/kg per minute for 5 h) with RU-486 (600 mg), during cortisol administration with a placebo, during 0.9% saline administration with RU-486, and during normal saline administration with a placebo. Clinicians administered a primed continuous infusion of D-[6,6-2H]glucose and [1-13C-]leucine during each test to determine hepatic glucose production and plasma leucine appearance rate. Continuous infusion of labeled bicarbonate in four men was also conducted to calculate the recovery factor of carbon dioxide in their breath. Researchers wanted to examine glucose and protein metabolism during hypercortisolemia with or without RU-486 and the effects of RU-486 on the metabolic effects of acute cortisol deficiency. Among men receiving the placebo, plasma glucose levels were higher during cortisol infusion than saline infusion (5.5 vs. 4.7 mmol/l; p 0.01). The leucine appearance rate was also higher during cortisol infusion than saline infusion (2.24 vs. 2 mcmol/kg per min; p 0.05) as well as leucine oxidation (0.51 vs. 0.31 mcmol/kg; p 0.01). Hepatic glucose production did not change in either placebo group. Cortisol did not induce the same metabolic changes when it was administered after RU-486. Normal saline infusion after RU-486 induced a short-term lower plasma glucose level and hepatic glucose production. Insulin, C-peptide, or glucagon did not change. Cortisol induced increased growth hormone (GH) levels (e.g., at 240 min, 5.9 vs. 1.7 mcg/l; p 0.01) while GH levels did not change when cortisol was administered after RU-486. These findings show that RU-486 suppresses the effects of acute hypercortisolemia on glucose and protein metabolism and GH secretion in males. Long-term studies could reveal the potential of RU-486 to prevent the adverse effects of chronic glucocorticoid administration. RU-486 allows researchers to study the metabolic effects of cortisol in males.
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PMID:RU 486 prevents the acute effects of cortisol on glucose and leucine metabolism. 788 13

Hydrocortisone was infused overnight into nine normal healthy adults on three occasions at 0, 80, and 200 micrograms.kg-1.h-1, producing plasma cortisol concentrations of 10.6 +/- 1.2, 34.0 +/- 2.0, and 64.9 +/- 4.3 micrograms/dl, respectively. L-[1-13C]leucine, L-[phenyl-2H5]phenylalanine, and L-[2-15N]glutamine were infused during the last 7 h of hypercortisolemia to measure amino acid kinetics. During the last 3.5 h, somatostatin, glucagon, and insulin were infused to reduce the cortisol-induced elevation in plasma insulin to basal. Hypercortisolemia increased plasma glucose, free fatty acid (FFA), and insulin concentrations. Institution of the somatostatin clamp returned insulin to basal but increased glucose and FFA. Acute hypercortisolemia increased protein breakdown 5-20%, as measured by increases in leucine and phenylalanine appearance rates. Normalizing insulin during hypercortisolemia did not alter phenylalanine flux but enhanced leucine appearance rate, the latter result indicating that insulin was affecting leucine metabolism during hypercortisolemia. The fraction of the leucine flux that was oxidized was not significantly increased with hypercortisolemia, but disposal by the nonoxidative route of leucine uptake for protein synthesis was increased. Hypercortisolemia increased cycling of amino acids by increasing protein breakdown and synthesis, but the increase in this process could have increased resting energy expenditure (REE) only 1-2%. Hypercortisolemia increased glutamine flux in a dose-dependent fashion through an increase in de novo synthesis, which presumably reflects increased release from skeletal muscle. Hypercortisolemia increased REE 9-15% at the 80 and 200 micrograms.kg-1.h-1 infusion rates. Respiratory quotient did not rise with cortisol infusion but tended to decrease, suggesting that the increase in REE was fueled by increased oxidation of fat. These data demonstrate that hypercortisolemia increases metabolic rate and may be in part responsible for the hypermetabolic state in injury.
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PMID:Effect of cortisol on energy expenditure and amino acid metabolism in humans. 790 Jul 96

Experiment 1 was conducted to characterize the concentrations of prolactin, growth hormone (GH), cortisol, insulin, glucagon, glucose, nonesterified fatty acids (NEFA), urea N, and 10 indispensable amino acids in the plasma of mares (n = 8) and stallions (n = 8) during the last 4 h of a 19-h period of feed deprivation and for 8 h after a noon meal. Experiment 2 was similar to Exp. 1 except that only stallions (n = 8) were used, and they were either fed (n = 4) or not fed (n = 4) at noon in a 2 x 2 Latin square design conducted over two sampling days 7 d apart. In Exp. 1, increases (P < .01) after feeding were observed for plasma concentrations of prolactin, cortisol, insulin, glucagon, glucose, urea N, and all amino acids except methionine; NEFA concentrations decreased (P < .01) after feeding. Episodic increases in GH concentrations were observed for most horses but were not associated with either feeding or gender (P > .1). Plasma urea N concentrations were higher (P < .025) overall in stallions than in mares, and the rise in prolactin concentrations after feeding was greater (P < .01) in stallions than in mares. In Exp. 2, meal-associated increases (P < .01) were observed for plasma concentrations of prolactin, insulin, glucagon, and glucose; NEFA concentrations decreased (P < .01). Except for cortisol, no hormone or metabolite varied with time across days when the stallions were not fed (P > .1), indicating that there was no inherent diurnal or feeding schedule-associated fluctuations in their concentrations. Cortisol concentrations varied (P < .02) over time but did not differ (P > .1) between fed and nonfed stallions. Again, GH concentrations were episodic but did not differ (P > .1) between fed and nonfed stallions. The lack of feeding effects on GH secretion in horses is similar to the response in pigs but differs from that in ruminants, in which GH concentrations generally decline after feeding.
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PMID:Changes in concentrations of hormones, metabolites, and amino acids in plasma of adult horses relative to overnight feed deprivation followed by a pellet-hay meal fed at noon. 807 Nov 78

The phenomenon of clinical improvement of diabetes mellitus after occurrence of pituitary insufficiency has been reported occasionally in the medical literature, as a human counterpart of Houssay's experiment with hypophysectomized diabetic animals. We report the case of a 76-year-old woman who developed diabetes in 1928, at the age of 14, and was treated with low doses of insulin. At the age of 29, during the 7th month of her second pregnancy, she suddenly developed severe headaches and soon afterwards an intense polyuria which subsided under treatment with posterior pituitary extract. Her pregnancy followed to term but uterine stimulants had to be used at delivery because of lack of contractions. She was unable to nurse her baby and a permanent amenorrhea ensued. She continued using the posterior pituitary powder for several years, after which she discontinued it without adverse effects. The dose of insulin was decreased gradually until its replacement by chloropropamide in 1967 and glibenclamide in 1970. The present dose of glibenclamide is 2.5 mg daily, on which she has occasional mild hypoglycemic reactions. When the medication was discontinued for 5 days glycemia rose to 450 mg/dl but responded immediately to 2.5 mg of the drug with a mild hypoglycemia. She never required thyroid hormone therapy. Glucocorticoid substitution was instituted recently because of evidence of mild adrenocortical insufficiency. Basal hormone levels were normal for thyroxin, thyrotropin, FSH, LH, prolactin, hGH and cortisol; the responses to pituitary stimulation with TRH and LHRH were subnormal or nil. Cortisol stimulation with ACTH was normal. Insulin levels rose moderately after stimulation with glucagon, and with glibenclamide, with simultaneous marked decrease in glycemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Houssay's phenomenon in man]. 820 16

The role of cortisol in directing the metabolic response to a combined infusion of glucagon, epinephrine, norepinephrine, and cortisol (stress hormones) was investigated. Chronically catheterized, conscious fasted dogs were studied before hormone infusion and after a 70-hour stress hormone infusion containing glucagon, epinephrine, norepinephrine, and cortisol (n = 11) or containing all these hormones except cortisol (n = 5). Combined stress hormone infusion increased arterial plasma glucagon, cortisol, epinephrine, and norepinephrine approximately sixfold. Whole-body glucose production (Ra), glycogenolysis, and gluconeogenesis were assessed using tracer and arteriovenous-difference techniques. The absence of an increase in cortisol during stress hormone infusion attenuated the increase in arterial plasma glucose concentration and Ra (delta 81 +/- 16 v 24 +/- 3 mg/dL and 1.7 +/- 0.3 v 0.8 +/- 0.4 mg/ kg/min, respectively). However, it did not alter the increase in net hepatic glucose output (delta 0.7 +/- 0.3 v 0.8 +/- 0.4 mg/kg/min). When the increase in cortisol was absent, the increase in net hepatic gluconeogenic precursor uptake was attenuated (delta 0.7 +/- 0.3 v 0.1 +/- 0.3 mg glucose/kg/min) due to a decrease in gluconeogenic precursor levels. The efficiency of gluconeogenesis increased to a greater extent (delta 0.19 +/- 0.07 v 0.31 +/- 0.11) when cortisol was not infused. The absence of an increase in cortisol also led to marked glycogen depletion in the liver (10 +/- 4 v 55 +/- 10 mg/g liver). Cortisol thus plays a pivotal role in the metabolic response to stress hormone infusion by sustaining gluconeogenesis through a stimulatory effect on hepatic gluconeogenic precursor supply and by maintaining hepatic glycogen availability.
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PMID:Role of cortisol in the metabolic response to stress hormone infusion in the conscious dog. 862 99

The aim of this study was to investigate the metabolic effects of abdominal versus vaginal hysterectomy with specific regard to perioperative glucose metabolism. Fourteen patients received either abdominal (AH, n = 7) or vaginal hysterectomy (VH, n = 7). Hepatic glucose production was measured before and 2.5 h after the operation by stable isotope technique ([6,6-2H2]-glucose). Metabolic substrates (glucose, lactate, nonesterified fatty acids [NEFA], beta-hydroxybutyrate) and hormones (insulin, glucagon, cortisol, catecholamines) were determined pre-, intra-, and postoperatively. VH induced a higher postoperative glucose concentration than the abdominal approach (VH, 148 +/- 25 mg/dL; AH, 111 +/- 16 mg/dL; P < 0.05). Since postoperative enhancement of hepatic glucose production was comparable in both groups, glucose clearance was lower after the vaginal procedure (VH, 1.7 +/- 0.3 mL.kg-1.min-1; AH, 2.1 +/- 0.3 mL.kg-1.min-1; P < 0.05). NEFA, beta-hydroxybutyrate, and catecholamines similarily increased after surgery. Cortisol levels were more increased after VH (VH, 80 +/- 26 micrograms/dL; AH, 37 +/- 14 micrograms/dL; P < 0.001). Lactate, glucagon, and insulin concentrations did not change perioperatively. The more pronounced hyperglycemic response to VH was due to lower peripheral glucose use caused by higher postoperative cortisol values. The mechanisms responsible for this marked cortisol enhancement after the vaginal operation as well as the clinical significance for patients with preexisting impaired carbohydrate tolerance, however, remained unclear and warrant further investigation.
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PMID:Influence of vaginal versus abdominal hysterectomy on perioperative glucose metabolism. 889 74

The aim of this study was to investigate metabolic changes during and after abdominal hysterectomy with specific regard to glycerol metabolism. Seven otherwise healthy patients with benign uterine myoma were enrolled in this study. Glycerol turnover and hepatic glucose production were measured before and after the operation by using stable-isotope technique ([1,1,2,3,3-2H5]-glycerol, [6,6-2H2]-glucose). Metabolic substrates (glycerol, nonesterified fatty acids, beta-hydroxybutyrate, glucose, lactate) and hormones (insulin, glucagon, cortisol, catecholamines) were determined pre-, intra- and postoperatively. Hysterectomy was associated with an increase of postoperative glycerol turnover from 3.56 +/- 1.28 to 6.46 +/- 2.44 mumol.kg-1.min-1 (P < 0.05). This increment was inversely related to the age of the patients (r = 0.872, P < 0.05). Glycerol concentration tended to increase perioperatively. These changes, however, were not of statistical significance. Hepatic glucose production and glucose plasma levels increased postoperatively from 9.75 +/- 1.61 to 12.79 +/- 1.45 mumol.kg-1.min-1 (P < 0.05) and 4.6 +/- 0.9 to 6.2 +/- 0.9 mmol/L (P < 0.05), respectively. Cortisol and catecholamine levels rose during and after surgery, while insulin and glucagon remained unchanged. The enhanced rate of lipolysis after hysterectomy was not detectable from plasma glycerol levels alone. The results of this study showed that using stable isotope technique allowed a more differentiated look at metabolic pathways than static plasma substrate concentrations, especially under perioperative conditions.
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PMID:Assessment of perioperative glycerol metabolism by stable isotope tracer technique. 913 77

101 male Wistar rats (body mass 180-200 g) received a single dose of ethanol in two concentrations--96% and 30%. High ethanol concentrations produced a direct damage to gastric and duodenal mucosa. 30% ethanol inhibited secretion of glucagon, insulin and aldosterone. This inhibition rapidly changes for the hormones rise in the blood. Hydrocortisone was high over the experiment. Previous intake of mineral water prevents damage to the gastroduodenal mucosa induced by 96% ethanol and modifies the hormonal response provoked by 30% ethanol as evident from reduced expression of the two phases.
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PMID:[The effect of the preliminary intake of mineral waters in acute alcoholic intoxication (an experimental study)]. 944 9


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