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)

Sodium nitroprusside was infused intravenously for 10 minutes in normal men, reclining at 45 degrees, in a dose sufficient to decrease the arterial pressure by 10 mmHg. The effect on a variety of plasma hormones was measured during the infusion and for 20 minutes afterwards. The heart rate increased to a maximum of 149%. Norepinephrine rose to a maximum of 196% in 5 minutes. Epinephrine reached a peak of 207% after 10 minutes. Plasma renin activity reached a peak of 449% at 10 minutes. Aldosterone did not change during the infusion, but increased to a maximum of 145% 10 minutes later. Vasopressin increased sharply at the end of the infusion to 893% and then rapidly decreased. Corticotropin, prolactin and growth hormone started to increase toward the end of the infusion, but reached their maxima during recovery. Corticotropin (225%) and prolactin (288%) peaked 10 minutes after the infusion, while growth hormone (414%) appeared still to be rising 20 minutes after the end of the infusion. Cortisol also rose progressively during recovery to a level of 138%. No significant changes were seen in the concentrations of insulin, glucagon, atrial natriuretic peptide, bombesin or neurotensin.
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PMID:Temporal relations of the endocrine response to hypotension with sodium nitroprusside. 155 71

Cell-to-cell communication via gap junctions has been proposed to be involved in the metabolic actions of sympathetic liver nerves in the rat. The effects of hepatic nerve stimulation and noradrenaline-, PGF2 alpha- and glucagon infusion on glucose metabolism and perfusion flow were studied in perfused rat liver in the absence and presence of the gap junctional inhibitors, heptanol, carbenoxolone and (4 beta)phorbol 12-myristate 13-acetate (4 beta PMA). (i) Stimulation of the hepatic nerve plexus increased glucose output, decreased flow and caused an overflow of noradrenaline into the hepatic vein. (ii) Heptanol completely inhibited not only the nerve stimulation-dependent metabolic and hemodynamic alterations but also the noradrenaline overflow. Thus the heptanol-dependent inhibitions were caused primarily by a strong impairment of transmitter release. (iii) Carbenoxolone inhibited the effects of neurostimulation on glucose metabolism partially by about 50%, whereas it left perfusion flow and noradrenaline overflow essentially unaltered. (iv) 4 beta PMA reduced the nerve stimulation-dependent enhancement of glucose release by about 80% but the noradrenaline-dependent increase in glucose output only by about 30%; the increase in glucose release by PGF2 alpha and by glucagon remained essentially unaltered. 4 beta PMA reduced the nerve stimulation-dependent decrease in portal flow by about 35% but did not affect the noradrenaline-and PGF2 alpha-elicited alterations, nor did it alter noradrenaline overflow. The results allow the conclusion that gap junctional communication plays a major role in the regulation of hepatic carbohydrate metabolism by sympathetic liver nerves, but not by circulating noradrenaline, PGF2 alpha or glucagon.
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PMID:Signal propagation via gap junctions, a key step in the regulation of liver metabolism by the sympathetic hepatic nerves. 157 64

The thermogenic effect of food and the rates of oxidation and storage of nutrients were evaluated by indirect calorimetry in 10 cirrhotic patients and seven normal controls for a 6-hour period, after they had consumed a standard meal supplying 15 kcal/kg body weight with 15%, 30%, and 55% protein, fat, and carbohydrate calories, respectively. Although the thermogenic response to food was not significantly lower in patients than in controls (51.6 +/- 13.5 v 72.2 +/- 8.8 kcal/6 h), patients exhibited a delayed and blunted increment of energy expenditure after the meal intake (P less than .025). The greater part of the glucose load was oxidized in patients (70.2 +/- 3.9% v 50.4 +/- 3.9% in controls; P less than .01), suggesting a defective glucose storage as glycogen. This result could be related to insulin resistance, which was evidenced by a large increase in glucose and insulin levels after the meal intake in patients (P +/- .001). Conversely, lipid oxidation was sharply reduced and de novo lipogenesis occurred in patients, so that the rate of lipid storage was increased. The profiles of circulating levels of catecholamines, thyroid hormones (free thyroxine [FT4] and triiodothyronine [T3]), and glucagon were assayed during the test. Norepinephrine and glucagon levels remained higher in patients throughout the test (P less than .001), whereas thyroid hormones stayed in the same range in the two groups. After an initial increase, glucose levels decreased sharply, inducing an activation of counterregulatory hormones, glucagon, and notably, epinephrine, for which the increment was correlated with the decrease of glucose (r = -.917; P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The thermogenic and metabolic effects of food in liver cirrhosis: consequences on the storage of nutrients and the hormonal counterregulatory response. 158 25

To determine whether specific hormonal responses were involved in the production of cryoprotectant (glucose) by liver of the freeze tolerant wood frog, Rana sylvatica, metabolically active hepatocytes were isolated in reasonable yields (mean 20.1 +/- 1.30% SEM, n = 29) by in situ liver perfusion with collagenase. Freshly isolated cells from autumn-collected frogs contained large amounts of glycogen (650 mumol glucosyl units/g packed cells) and produced glucose from this endogenous reserve at a rate of 10 mumol g-1 hr-1 at 0 degrees. Glucose output from cells was highly responsive to the addition of hormones; rates of glucose release increased 2.1-, 1.7-, and 1.7-fold with the addition of 10(-7) M bovine glucagon, 10(-7) M epinephrine, and 5 x 10(-6) M dibutyryl-cyclic AMP, respectively. Norepinephrine, 5-hydroxytryptamine, and bovine insulin were without effect at 0.1 microM/l. Hormone stimulation of glucose release was correlated with an increase in both the total activity and the percentage a of glycogen phosphorylase in hepatocytes. However, none of the hormones tested affected the kinetic properties of hepatocyte pyruvate kinase, suggesting the absence of covalent modification control of the enzyme. The data indicate that the freezing-stimulated production of large quantities of glucose as a cryoprotectant by R. sylvatica liver does not involve qualitative differences in the hormonal control of liver glycogenolysis, compared with other lower vertebrates. However, quantitative differences were seen, such as the much greater phosphorylase activity, 4.38 +/- 0.33 mumol min-1 g-1 packed cells, in freshly isolated R. sylvatica hepatocytes compared with 0.36 +/- 0.06 mumol min-1 g-1 in Rana pipiens hepatocytes.
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PMID:Hormonal effects on glycogen metabolism in isolated hepatocytes of a freeze-tolerant frog. 162 97

The in vitro brown adipose tissue (BAT) oxygen consumption stimulated by noradrenaline (NA) or glucagon (G) was significantly lower in chronically NA-treated rats and that of G-treated rats did not differ as compared with that of vehicle-treated control animals. In vitro thermogenic response of BAT in NA-treated rats was consistent with that induced by cold acclimation.
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PMID:Effects of chronic administration of noradrenaline and glucagon on in vitro brown adipose tissue thermogenesis. 162 78

Brown adipose tissue (BAT) is a major site of nonshivering thermogenesis (NST) during cold acclimation for most mammals. Repetitive nonthermal stress such as immobilization has been shown to enhance the capacity of NST as cold acclimation. In the present study, the effects of running training, another type of nonthermal stress, were investigated on in vitro thermogenesis and the cellularity of interscapular BAT in rats. The rats were subjected to treadmill running for 30 min daily at 30m/min under 8 degrees inclination for 4-5 weeks. In vitro thermogenesis was then measured in minced tissue blocks incubated in a Krebs-Ringer phosphate buffer containing glucose and albumin at 37 degrees C, using a Clark type oxygen electrode. The trained rats showed less body weight gain during the experiment. The weights of BAT and epididymal white adipose tissue were smaller in the trained rats. Noradrenaline- and glucagon-stimulated oxygen consumption were also significantly smaller in the trained rats. The tissue DNA level was greater in the trained rats, but the DNA content per tissue pad did not significantly differ. The results indicate that running training reduces BAT thermogenesis, possibly as an adaptation to conserve energy substrates for physical work.
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PMID:Effects of running training on in vitro brown adipose tissue thermogenesis in rats. 163 84

1. The effect of moderate endurance exercise on blood glucose concentration and on glucoregulatory hormones was studied in nine thyrotoxic and five myxoedematous humans before and 3 months after anti-thyroid and substitution therapy, respectively. 2. At rest, the fasting concentrations of insulin and pro-insulin correlated positively with the prevailing total tri-iodothyronine concentration, whereas the concentrations of noradrenaline and cortisol correlated inversely with the tri-iodothyronine concentration. 3. During exercise the plasma insulin, pro-insulin and C-peptide concentrations decreased. The plasma glucagon concentration increased slightly in thyrotoxic patients before and after treatment and was largely unchanged in myxoedematous patients in either state. 4. The plasma noradrenaline concentration increased before and after treatment in both groups, with concentrations two times higher in the myxoedematous than in the thyrotoxic patients. Treatment for 3 months did not change this pattern. The plasma adrenaline concentration increased in both groups, but in the untreated thyrotoxic patients the increase was two to three times greater than that after treatment or that in the myxoedematous group. 5. The blood glucose concentration decreased in eight of nine untreated thyrotoxic patients, but was largely unchanged after treatment or in the myxoedematous patients. A strong negative correlation was found between the decline in blood glucose concentration and the increase in plasma adrenaline concentration in the thyrotoxic group. 6. Thus, during exercise untreated thyrotoxic patients are prone to hypoglycaemia, show an inadequate glucagon response, and exhibit a large counter-regulatory increase in plasma adrenaline concentration.
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PMID:Responses of glucose and glucoregulatory hormones to exercise in thyrotoxic and myxoedematous patients before and after 3 months of treatment. 164 30

1. The effect of hyperketonaemia on counter-regulatory hormone responses to hypoglycaemia has been examined in six healthy subjects. 2. A controlled, step-wise reduction in blood glucose concentration was achieved by adjusting the rate of glucose infusion during a primed-continuous infusion of soluble insulin (1.5 m-units min-1 kg-1 body weight, plasma insulin concentration approximately 90 m-units/l). Simultaneous infusion of either saline or beta-hydroxybutyrate (3 mg min-1 kg-1 body weight) was administered in a single-blind fashion, in random order. Despite a need for 40% more glucose during the ketone infusion, an identical fall in blood glucose concentration was achieved in each study. 3. The glycaemic threshold for stimulating an adrenaline response of 0.41 nmol/l was reduced from 3.1 to 2.8 mmol/l (P less than 0.05) during ketone infusion, and that for stimulating a response of more than 50% of basal from 3.6 to 3.1 mmol/l (P less than 0.001). The peak adrenaline response fell from 7.97 to 2.6 nmol/l (P less than 0.04). Peak noradrenaline, cortisol and growth hormone responses were also significantly lower during ketone infusion (P = 0.04, 0.001 and 0.006, respectively). Glucagon responses alone were unaffected by hyperketonaemia. 4. The provision of an alternate metabolic fuel thus produced immediate changes in the neurohumoral responses to hypoglycaemia. This is consistent with the hypothesis that human nervous tissue can metabolize ketones acutely.
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PMID:Ketone infusion lowers hormonal responses to hypoglycaemia: evidence for acute cerebral utilization of a non-glucose fuel. 165 62

1. Adrenal responses to intra-aortic infusions of acetylcholine (4.5 nmol min-1 kg-1 for 10 min) have been investigated in conscious, functionally hypophysectomized, 3- to 6-week-old calves, in the presence and absence of exogenous ACTH (2 ng min-1 kg-1, I.V.). 2. Acetylcholine produced a substantial fall in adrenal vascular resistance, which was significantly reduced in the presence of exogenous ACTH, while producing minimal changes in aortic blood pressure and heart rate. 3. There was also a significant rise in right adrenal cortisol output which was sufficient to produce a measurable rise in plasma cortisol concentration. The effect could be accounted for by the increase in adrenal ACTH presentation. It was abolished by pre-treatment with atropine (0.2 mg kg-1). A small but significant rise in aldosterone output during acetylcholine infusions was also abolished in the presence of ACTH. 4. Both adrenaline and noradrenaline were released during intra-aortic acetylcholine infusions and these responses were substantially reduced, but not abolished, by pre-treatment with atropine. 5. Acetylcholine also stimulated the release of corticotrophin-releasing factor (CRF) and [Met5]enkephalins from the gland. The output of CRF was enhanced and that of free [Met5]enkephalin was significantly reduced in the presence of exogenous ACTH. All these responses were largely, but not completely, suppressed by atropine. 6. Acetylcholine also promoted the release of the pancreatic hormones glucagon, insulin and pancreatic polypeptide (PP). The amounts of pancreatic glucagon and insulin that were released were highly dependent on the concentration of glucose in the circulating plasma and all these responses were abolished by atropine. 7. It is concluded that acetylcholine is capable of stimulating the release of a wide variety of agonists from the adrenal gland when infused intra-aortically at a dose of 4.5 nmol min-1 kg-1. The increase in cortisol output appears to be secondary to an increase in blood flow whereas the adrenal medullary responses are not, and appear to be due largely, but not entirely, to activation of muscarinic receptors.
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PMID:Endocrine responses to intra-aortic infusions of acetylcholine in conscious calves. 165 16

1. Splanchnic haemodynamic changes were studied in seven healthy subjects during hypoglycaemia induced by the intravenous infusion of insulin. Superior mesenteric artery blood flow and cardiac output were examined noninvasively by a Doppler ultrasound technique. 2. Blood glucose concentration fell from 4.5 (0.14) mmol/l basally to 1.5 (0.09) mmol/l [mean (SEM), P less than 0.003] at the hypoglycaemic reaction ('R') and recovered to baseline by 'R' + 60 min. There was an associated rise in plasma glucagon, adrenaline and noradrenaline levels. 3. Superior mesenteric artery blood flow rose at 'R' from a basal value of 532 (38) ml/min to a peak of 803 (73) ml/min at 'R' + 10 min [mean (SEM), P less than 0.005] and remained significantly elevated until 'R' + 40 min. Resistance in this vessel fell by 33% at 'R' + 10 min (P less than 0.005) and remained significantly low until 'R' + 40 min. 4. Cardiac output rose by 33% at 'R' (P less than 0.004) and returned to normal by 'R' + 20 min. This was associated with a 24% rise in pulse rate (P less than 0.03), but no change in stroke volume or mean arterial pressure. Total peripheral resistance fell by 21% at 'R' (P less than 0.005) and had returned to normal by 'R' + 20 min. 5. The sustained rise in splanchnic blood flow during hypoglycaemic recovery may be of homoeostatic importance by providing metabolic fuel to the liver for gluconeogenesis.
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PMID:Splanchnic haemodynamic changes during acute hypoglycaemia in man. 165 99


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