Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Some insulin-dependent diabetic patients who have clear symptoms of hypoglycaemia during animal insulin treatment have reported loss of these symptoms when human insulin preparations are introduced. A survey of Mersey Region, UK, identified eleven patients whose awareness of hypoglycaemia was lost after introduction of human insulin but returned with animal insulin treatment; seven took part in the study. Acute hypoglycaemia was induced in these patients on two occasions by intravenous infusion of porcine or human soluble insulin (2.5 mU.kg-1, min-1) in random order. There was no significant difference between porcine and soluble insulin in the plasma glucose profile; mean (SEM) plasma glucose fell from 7.1 (0.4) mmol/l to a nadir of 1.5 (0.1) mmol/l with porcine insulin and from 7.1 (0.5) mmol/l to 1.6 (0.2) mmol/l with human insulin. An acute autonomic reaction occurred in all seven patients, at a similar plasma glucose concentration (1.9 [0.1] mmol/l with porcine insulin; 2.0 [0.2] mmol/l with human insulin). There were no significant differences in the frequency of symptoms or signs of hypoglycaemia between the two insulin species, nor any consistent differences in plasma glucagon, cortisol, growth hormone, adrenaline, or noradrenaline responses to hypoglycaemia. Symptomatic and hormonal responses to acute hypoglycaemia induced by porcine and human soluble insulins therefore seem to be almost indistinguishable, even in patients carefully selected for their apparent loss of hypoglycaemia awareness with human insulin.
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PMID:Human insulin and awareness of acute hypoglycaemic symptoms in insulin-dependent diabetes. 168 Dec 96

In an attempt to clarify whether circulating insulin per se exerts an inhibitory effect on the hormonal responses to hypoglycemia, with special emphasis on glucagon secretion, nine healthy volunteers were exposed to low dose (244 pmol/kg.h) and high dose (1034 pmol/kg.h) iv insulin infusions for 3 h on two separate occasions. A close to identical arterial hypoglycemia of about 3.4 mmo/L was obtained in both tests by glucose clamping during the high dose test. The corresponding glucose concentration in the venous blood was significantly lower in the high dose test (2.5 +/- 0.1 vs. 3.0 +/- 0.1 mmol/L; P less than 0.01), while the plasma free insulin level was 4 times higher in the high dose test (897 +/- 50 vs. 208 +/- 14 pmol/L). Plasma glucagon was elevated in both experiments, but its rise was reduced during the high dose test after 1 h, yielding an incremental area under the glucagon curve that was significantly smaller than that obtained during the low dose test (213 +/- 70 vs. 348 +/- 81 ng/L.h; P less than 0.05). The plasma adrenaline, noradrenaline, GH, C-peptide, pancreatic polypeptide, and somatostatin profiles were similar in the two tests. We conclude that an inhibitory effect of circulating insulin on the glucagon response to hypoglycemia can be demonstrated in normal man during an infusion of insulin yielding a plasma concentration of about 900 pmol/L. The responses of other hormones studied are not significantly influenced by the circulating insulin level.
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PMID:A high concentration of circulating insulin suppresses the glucagon response to hypoglycemia in normal man. 168 39

Vanadate has been shown to improve glucose homoeostasis in mildly glucose-intolerant and severely insulin-resistant fa/fa rats. The present study examined whether changes in insulin counter-regulatory hormones contribute to this beneficial effect of vanadate. Since oral administration of Na3VO4 caused a decrease in food intake and stopped the increase in body weight, vanadate-treated fa/fa rats were compared with both controls with food available ad libitum and pair-fed rats. Slightly lower plasma glucose levels were maintained in conjunction with markedly lower plasma insulin levels in vanadate-treated rats, and this effect was not simply due to the smaller body weight of the animals. Compared with control rats, treatment with vanadate affected neither basal plasma glucagon levels nor the increase in glucagon levels observed after insulin-induced hypoglycaemia or after i.v. injection of arginine. Compared with pair-fed rats, treatment with vanadate prevented the fall in basal plasma glucagon and its exaggerated rise in response to insulin that mere food restriction produced. Plasma corticosterone levels were high in fa/fa rats. Vanadate and pair-feeding similarly decreased basal plasma levels of corticosterone as well as nocturnal corticosteronuria. Thus the attenuation of the hypercorticism of fa/fa rats results from the reduction in body weight gain rather than from a specific action of vanadate. Vanadate did not influence urinary excretion of noradrenaline, an index of neural sympathetic activity, but prevented the increase in adrenaline excretion, an index of adrenal medulla activity, that was produced by food restriction in pair-fed rats. In conclusion, vanadate administration has no or little specific effects on three major insulin counter-regulatory hormones. This reinforces the suggestion that the beneficial effects of vanadate on glucose homoeostasis in fa/fa rats are mainly due to a correction of insulin resistance in peripheral tissues.
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PMID:The influence of vanadate on insulin counter-regulatory hormones in obese fa/fa rats. 174 66

Immunological implications are important in every surgical operation, specially when it is necessary to remove the spleen. She plays an important role in immunological aspecific (filter, phagocytosis) and specific processes (production of IgM and regulation of T- and B-lymphocytic system). Splenectomy causes an immunodeficiency with frequent post-operative complications (the most important is OPSI). Each operated patient is considered generically immunodeficient because surgical trauma and anesthesiologic practice are at the base of immunological alterations (biological barriers, aspecific immunity, A.P.P., complement, specific immunity, NK cells). It's indispensable to know pathological situations that make "critical" the immunological state: caloric-proteic malnutrition, elderly (greater than 70 years old), immunosuppressive therapy, sepsis, shock, neoplasms. I. e.: a patient about seventy years old presents a reduced endocrine secretion of thymic hormone and, probably, a low synthesis of immunoglobulins. Besides the corticosteroids modify the answer of T-lymphocytes and NK cells. Sepsis induces metabolic and immunological alterations after early activation of humoral mediators, modified quantity and life of A.P.P., activation of complement, inhibition of cell-mediate immunity, modification of number and activity of haematic lymphocytes. Trauma induces a hypersecretion of corticosteroid, adrenalin, noradrenaline, glucagon with consequent hypercatabolism that causes malnutrition. The hormonal hypersecretion is a determining factor of reduced phagocytic activity (inhibited migration of neutrophils and monocytes), quantitative and qualitative alterations of complement, deficit of T-cells, hyporeactivity to skin test, depressed answer of antibodies to bacterial and viral antigens. Progressive neoplasms are characterized by modification of T-lymphocytes number, depressed macrophagic activity, hyporeactivity to skin tests.
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PMID:[Immunological implications of surgical intervention in critical and noncritical patients]. 175 43

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 purpose of the study was the assessment of certain biological effects of semisynthetic human insulin compared with the presently used monocomponent preparations of porcine insulin made by the same producer. The study was carried out in a group of 10 healthy subjects (7 men and 3 women) twice: during a loading test with porcine insulin, and then during a similar test with human insulin. Both insulins were administered intravenously in doses of 0.075 units/kg body weight The physiological reactions associated with hypoglycaemia were noted, including subjective experiences and hormonal responses, among them those of glucagon, growth hormone, prolactin, adrenaline, noradrenaline and C-peptide. Semisynthetic human insulin administered intravenously was found to exert an identical hypoglycaemic effect as porcine insulin. However, it was observed that the action of porcine insulin was associated with more pronounced symptoms and more intense physiological reactions (tachycardia, body temperature fall) and a striking increase of prolactinaemia, in relation to semisynthetic human insulin.
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PMID:[Comparative assessment of the biological effects of semisynthetic human insulin and porcine insulin in healthy subjects]. 181 87

We found that glucagon stimulated membrane protein kinase C (PKC) activity and phosphatidylcholine hydrolysis in 24 h-cultured rat hepatocytes. Phorbol myristate acetate, 8-bromo cyclic AMP, vasopressin, noradrenaline and the Ca2+ ionophore A23187 also stimulated membrane PKC activity. However, only vasopressin and noradrenaline stimulated inositol phosphate accumulation, whereas all agonists stimulated the rate of release of water-soluble choline metabolites into the medium. Choline, and to a much lesser extent phosphocholine, were released, suggesting predominantly phospholipase D activation. This was supported by the finding that the accumulation of phosphatidate and diacylglycerol was enhanced by the agents in [3H]myristate-labelled hepatocytes, as was [32P]phosphatidylethanol formation. Since the time courses for the release of choline into the medium and the accumulation of phosphatidate and diacylglycerol caused by vasopressin and glucagon were similar, the more rapid activation of PKC by vasopressin probably reflects diacylglycerol formation from phosphoinositide breakdown. The inability of glucagon to stimulate inositol phosphate production was not due to the prolonged culture, since similar results were obtained in 4 h cultures. We conclude that the stimulation of membrane PKC activity by glucagon correlates with accumulation of diacylglycerol and phosphatidate derived from the hydrolysis of phosphatidylcholine.
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PMID:Activation of membrane protein kinase C by glucagon and Ca(2+)-mobilizing hormones in cultured rat hepatocytes. Role of phosphatidylinositol and phosphatidylcholine hydrolysis. 185 65

The effect of fasting on hepatic endothelial lipase activity in the liver of adult rats was investigated. We found that, both in male and female rats, fasting produced a progressive decrease of the hepatic endothelial lipase activity. Upon refeeding, the activity returned to control values in 48 h. In isolated livers from fed male rats, a sharp peak of hepatic endothelial lipase activity appeared in the perfusate upon heparin addition. It accounted for 75% of the total activity (heparin-released + residual) of the tissue. Fasting (24 h) decreased the heparin-releasable activity, and this effect was responsible for most of the decrease found in whole tissue. We suggest that the effect might be due to a decreased synthesis and/or secretion of the enzyme by hepatocytes, since isolated hepatocytes from fasted rats, incubated at 37 C, released 65% less activity to the incubation medium than hepatocytes from fed rats. Adrenaline, but not insulin, glucagon, dexamethasone, epidermal growth factor, or T3, decreased the amount of hepatic endothelial lipase activity released by hepatocytes isolated from fed rats. The effect of adrenaline appears to be mediated by alpha 1-receptors since phenylephrine but not isoprenaline reproduced, and prazosin but not propranolol blocked, the effect of the catecholamine. In the presence of cycloheximide, adrenaline also decreased the amount of activity released. We suggest that, in our incubation conditions (up to 3 h), the hormone affects the posttranslational processing of the enzyme. In vivo administration of prazosin blocked the effect of both noradrenaline and fasting on hepatic endothelial lipase activity in whole liver. Those results suggest that catecholamines are involved in the decreased hepatic endothelial lipase activity found in the liver of fasted rats, and points out the role of these hormones in the acute modulation of an enzyme involved in reverse cholesterol transport.
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PMID:Involvement of catecholamines in the effect of fasting on hepatic endothelial lipase activity in the rat. 193 90

To assess compensation for the absence of the exercise-induced fall in insulin, dogs underwent 150 min of treadmill exercise with insulin infused intraportally with (IC + Glc; n = 7) or without (IC; n = 6) glucose clamped. Glucose production (Ra), gluconeogenic conversion (Conv), and intrahepatic gluconeogenic efficiency (Eff) were assessed with tracers ([3H]glucose, [14C]alanine) and arteriovenous differences. Glucose fell by 6 +/- 4 and 11 +/- 2 mg/dl at 30 min of exercise and by 8 +/- 2 and 36 +/- 5 mg/dl at 150 min in IC + Glc and IC. Glucagon rose by 16 +/- 8 and 55 +/- 17 pg/ml by 30 min of exercise and by 18 +/- 6 and 93 +/- 22 pg/ml by 150 min in IC + Glc and IC. Norepinephrine was unaffected by the glycemic decrement in IC, whereas epinephrine was greater for the last 60 min of exercise. Ra rose by an average of 0.9 +/- 0.3 and 3.7 +/- 0.2 mg.kg-1.min-1 in IC + Glc and IC. Conv rose by 91 +/- 39 and 325 +/- 75% in IC + Glc and IC at 150 min of exercise, and Eff rose by 87 +/- 57 and 358 +/- 99%. The compensatory Ra exceeded the maximum possible gluconeogenic rate, indicating that glycogenolysis was also stimulated. In summary, in the absence of the exercise-induced fall in insulin 1) glycemia falls approximately fourfold faster; 2) minimal glycemic decrements elicit a large and rapid increase in Ra; 3) this compensation involves a glycogenolytic and gluconeogenic response; 4) the accelerated gluconeogenic rate is due, in large part, to stimulation of Eff; and 5) the compensatory Ra is likely mediated, in part, by glucagon. Hence, although the fall in insulin is essential for normal glucoregulation during exercise, a highly sensitive counterregulatory response prevents severe hypoglycemia. The remarkable sensitivity of the liver to small changes in glycemia implies that the normal coupling of the exercise-induced increase in Ra to glucose utilization may be signaled by small, nearly imperceptible changes in glucose.
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PMID:Efficiency of compensation for absence of fall in insulin during exercise. 195 83

Norepinephrine (NOR) is a potent activator of carbohydrate metabolism in isolated hepatocytes from copper rockfish (Sebastes caurinus), increasing rates of glycogenolysis fourfold with an EC50 of 6.3 nM. Nanomolar concentrations of NOR also enhance gluconeogenesis. Epinephrine (EPI) activates both pathways to a smaller extent; the corresponding EC50 for glycogenolysis is 320 nM. There is no significant difference between the magnitude of glucose production in response to comparable doses of NOR, bovine glucagon, and catfish glucagon-like peptide. Experiments with an adrenergic agonist (isoproterenol) and antagonists (propranolol, prazosin, atenolol) indicate that NOR effects are mediated through beta-adrenoceptors. Catecholamine-activated glycogenolysis measured at 100 nM EPI or NOR is poorly correlated with a 30-50% rise in intracellular cAMP. Glucose production following catecholamine administration is not linear: 50% of the hourly glucose output is released within the first 17 min (NOR) and 5 min (EPI), respectively. During hepatocyte incubation (60 min at 15 degrees), added NOR and EPI (100 nM) were not degraded to any significant extent. In the absence of added hormones, rockfish hepatocytes produce 7.41 +/- 0.89 mumol glucose x g-1 packed cells x hr-1 at 15 degrees, with gluconeogenesis accounting for 35.0% of the total production. The rate of glucose output, which is linear for at least 60 min, is not correlated with the initial hepatocyte glycogen level.
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PMID:Norepinephrine: a potent activator of glycogenolysis and gluconeogenesis in rockfish hepatocytes. 197 May 44


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