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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anesthesia, surgical trauma, heparinization, priming volume composition, and temperature control of the heart-lung machine individually affect carbohydrate, protein, or lipid metabolism during cardiac operations. The impact of some of these factors on glucose and insulin regulation was assessed before, during, and after normothermic cardiopulmonary bypass in nondiabetic patients with use of a servo-controlled insulin delivery system. With a glucose-free prime, cardiopulmonary bypass induced a slight hyperglycemia but no endogenous insulin response, suggesting a partial inhibition of insulin secretion. Nonetheless, insulin release could be stimulated by exogenous glucagon. A glucose load in the priming fluid led to marked and persistent hyperglycemia without commensurate insulin release. Elevated stress hormone levels, a concomitant reduction of insulin release and insulin action, and a depression of peripheral glucose utilization, as demonstrated by glucose clamp experiments, contributed to these perturbations of glucose and insulin metabolism. Although the metabolic alterations observed are not critical in routine cardiac operations, they may become clinically significant in postoperative states with unusual persistence of stress conditions.
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PMID:Alterations of insulin and glucose metabolism during cardiopulmonary bypass under normothermia. 388 Aug 48

Little is known of the endocrine and metabolic milieu in preterm and term neonates exposed to surgical stress. In order to define the effects of anaesthesia and surgery on the hormonal regulation of intermediary metabolism, the levels of plasma insulin, glucagon, adrenaline and noradrenaline were measured in addition to blood glucose, lactate, pyruvate, alanine, acetoacetate, hydroxybutyrate, glycerol and plasma-free fatty acids in 38 neonates (23 term, 15 preterm) undergoing surgery. Blood samples were drawn pre-operatively, at the end of surgery, and at 6, 12 and 24 h post-operatively. Plasma levels of adrenaline and noradrenaline increased significantly in response to surgery. In term neonates, plasma insulin concentrations were unaltered at the end of surgery, but were significantly increased throughout the post-operative period; plasma glucagon levels were unchanged at the end of surgery but had significantly decreased by 24 h after surgery. Insulin levels in preterm neonates remained unchanged during surgery as well as in the post-operative period. All neonates developed a significant peri-operative hyperglycaemia which persisted up to 12 h after surgery. Blood lactate and pyruvate increased during surgery, accompanied by significant increases in plasma free fatty acids, total ketone bodies and glycerol concentrations by the end of surgery. Blood glucose concentrations were significantly correlated with plasma adrenaline levels at the end of surgery and with plasma glucagon at 6 h post-operatively. The insulin/glucose ratio was significantly decreased at the end of surgery in term and preterm neonates. Further analysis showed that total parenteral nutrition given just before surgery and thiopentone anaesthesia given during surgery significantly augmented the peri-operative hyperglycaemic response of term neonates. Thus, stress-related hormonal changes in preterm and term neonates may precipitate a catabolic state characterized by glycogenolysis, gluconeogenesis, lipolysis and mobilization of gluconeogenic substrates in the post-operative period. Prevention of these metabolic derangements by anaesthetic or hormonal manipulation may possibly help to improve the clinical outcome of neonates undergoing surgery.
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PMID:Studies on the hormonal regulation of fuel metabolism in the human newborn infant undergoing anaesthesia and surgery. 392 73

The influences of IAP on the residual pancreatic endocrine function and carbohydrate metabolism after extensive pancreatectomy in the rat were studied with oral glucose tolerance test (OGTT), arginine tolerance test (ATT), and measurement of hepatic glycogen, and hepatic glycolytic enzyme activity, and histological examination, etc. Wistar male rats weighing around 300 g were divided into the groups with IAP treatment and without it, and in the group with IAP treatment IAP 10 micrograms/kg was administered without anesthesia via the tail vein. In each group 60 and 90% pancreatectomies were performed in accordance with Scow's method, and the simple laparotomy group was used as control. Slight abnormality of glucose tolerance was shown in 60% pancreatectomy. The abnormality became worse with time in 90% pancreatectomy. Glucagon secretion was not damaged markedly even after extensive pancreatectomy. IAP stimulated IRI secretory response and improved glucose tolerance in 60% pancreatectomy group. IAP showed no effect in 90% pancreatectomy group. IAP did not stimulate IRG secretory response after pancreatectomy. Hepatic glycolytic enzyme activity was high in the group with IAP treatment. From the above observation, it has been suggested that IAP may be indicated for the abnormal carbohydrate metabolism after pancreatectomy, if pancreatectomy is not too extensive.
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PMID:[Experimental study on carbohydrate metabolism and pancreatic endocrine function after pancreatectomy--influence of islet activating protein (IAP)]. 396 25

1. The extent to which the autonomic innervation to the pancreas is implicated in the control of glucagon release during hypoglycaemia has been investigated in calves 3-6 weeks after birth.2. A pronounced rise in plasma glucagon concentration occurred in normal conscious calves in response to hypoglycaemia following administration of insulin (0.1 u./kg). Prior treatment with atropine caused no significant change in the hypoglycaemic response to insulin in these animals but the rise in plasma glucagon concentration was delayed.3. Section of both splanchnic nerves produced no significant change in the tolerance of conscious calves to this small dose of insulin and the changes in plasma glucagon concentration in these animals were within the normal range.4. In contrast, the same dose of insulin produced severe hypoglycaemia, accompanied by convulsions, in atropinized calves with cut splanchnic nerves. In spite of the intensity of the hypoglycaemic stimulus the rise in plasma glucagon concentration was both delayed and diminished in these animals.5. Administration of atropine alone (0.2 mg/kg) to normal fasting calves produced a significant fall in the mean plasma concentrations of both glucose and glucagon (P < 0.01) within 30 min, without affecting that of insulin.6. A significant increase in plasma glucagon concentration also occurred in response to stimulation of the peripheral ends of the thoracic vagi in adrenalectomized calves with cut splanchnic nerves under barbiturate anaesthesia. A rise in mean plasma glucose concentration was also observed in these experiments and found to be significantly correlated with the glucagon response.7. It is concluded that changes in either sympathetic or parasympathetic efferent activity may modify plasma glucagon concentration in the conscious calf, but that only the latter mechanism is likely to be implicated in the response to changes in plasma glucose concentration within the physiological range.
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PMID:The role of the autonomic innervation in the control of glucagon release during hypoglycaemia in the calf. 482 77

1. Administration of glucagon to foetal rats produced a 10-15-fold increase in hepatic phosphoenolpyruvate carboxykinase activity together with a similar increase in the overall pathway of pyruvate conversion into glycogen in liver slices. 2. Glucagon was without effect on gluconeogenesis in vivo, which remained at approx. 0.1% of the incorporation as measured in newborn animals. 3. The apparent discrepancy between these results was due to the ether anaesthesia that was required for experimentation in vivo. Under conditions when minimal ether was used, the rates of labelling of glycogen from [3-(14)C]pyruvate in vivo were increased 10-20-fold and there was an additional stimulus by glucagon. 4. Ether anaesthesia produced a more reduced redox state of the foetal liver cytosol and lowered the ATP/ADP concentration ratio. 5. It is proposed that these effects are significant in the limitation of gluconeogenesis in the foetal rat liver, so that only with high phosphoenolpyruvate carboxykinase activity, high ATP concentration and a relatively oxidized cytosol redox state will a functional gluconeogenic pathway be present.
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PMID:The development of gluconeogenesis in rat liver. Effects of glucagon and ether. 549 60

In a prospective randomised study, 47 fasting women undergoing elective caesarean section received one of the following three glucose regimens for prevention of hypotension before administration of epidural bupivacaine to produce anaesthesia from the T4 sensory level: (i) 150 ml of 5% dextrose in water (D5W) and 1000 ml normal saline (7.5 g dextrose); (ii) 150 ml of D5W, 350 ml of 5% dextrose in normal saline (D5NS), and 650 ml of normal saline (25 g dextrose); (iii) 150 ml D5W and 1000 ml D5NS (57.5 g dextrose). The maternal blood sugar at delivery was significantly raised in patients receiving 25 and 57.5 g of dextrose. 57.5 g of dextrose also raised the mean umbilical cord venous levels of glucose to 11.7 mmol/l and of insulin to 70 +/- 7 microU/ml, while decreasing glucagon to 24 +/- 5.3 pg/ml and arterial pH to 7.19 +/- 0.015 compared with the levels with 7.5 g dextrose. The raised insulin level caused neonatal hypoglycaemia (1.8 +/- 0.22 mmol/l) and delayed release of glucagon at 2 hours of age. There was a higher incidence of neonatal jaundice in infants exposed to 57.5 g of dextrose than in those exposed to 7.5 g. The addition of large amounts of dextrose to intravenous fluids was harmful to the fetus and of no benefit to the mother. Until a safe rate of administration is established, it is recommended that dextrose infusions immediately before delivery be limited to no more than 6 g/h.
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PMID:Fetal and neonatal hazards of maternal hydration with 5% dextrose before caesarean section. 612 39

Short-lasting hypothermia during thiobutabarbital general anaesthesia causes no decrease of the absolute ATP level in the blood and liver of rats. The adenylate energy charge in the tissues is relatively high - 0.86 in the liver and 0.85 in the muscles, which might be an evidence of a significant "energy sparing" during moderate hypothermia (26 +/- 1 degree C). Somatostatin in a dose of 20 micrograms/kg of body weight given to the rats during hypothermia decreased the ATP level, the ATP/ADP ratio and the adenylate energy charge in the studied tissues, especially in the liver, evidencing increased intensity of catabolic processes caused by the inhibitory action of somatostatin on the release of insulin and glucagon, among other hormones, and on the change of the insulin/glucagon ratio.
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PMID:Somatostatin effect on the level of adenyl nucleotides in the blood and tissues of rats during short-lasting hypothermia. 614 95

The occurrence of an anaphylactoid shock in a patient treated with beta-adrenergic blocking agents during a long time prior to surgery constitutes a high risk because beta-receptors are refractory to adrenergic substances and compensatory mechanisms are obtunded. The shock is characterized by severe hypotension and bradycardia, both resistant to adrenaline. These signs were observed in a patient treated with metoprolol for hypertension several months prior to surgery. The intravenous injection of an iodine containing contrast medium during general anaesthesia was followed by a lethal anaphylactoid shock resistant to adrenaline, atropine and isoprenaline. The treatment of the shock needs, besides adrenaline, massive vascular filling, high doses of beta-agonists and glucagon.
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PMID:[Fatal anaphylactic shock in a patient treated with beta-blockers]. 615 72

In adult male SPF rats anaesthetized with pentobarbital and subjected to traumatization in revolving Noble-Collip drums for 2 min (= 120 revolutions) maximal increases of liver glycogen phosphorylase activity were observed. In experiments on rats with permanent arterial catheters for blood sampling no posttraumatic increase of plasma norepinephrine and an only slight increase of plasma epinephrine was observed if the animals were traumatized under anaesthesia, in contrast to the considerable increases in the plasma level of both hormones in rats subjected to the injury without anaesthesia. Time and extent of the phosphorylase response of anaesthetized rats after trauma were compared with changes in enzyme activity after i.v. administration of exogenous epinephrine or glucagon. A nearly maximal response after 1 microgram kg-1 epinephrine was present within 1 min, whereas after 0.1 micrograms kg-1 of glucagon there was comparable phosphorylase activation 2 min after administration of the hormone. The plasma renin-angiotensin activity was not increased after injury for 2 min under anaesthesia so that only the increase in plasma vasopressin fitted in with the criteria for possible activators of phosphorylase. An additional role of glucagon also cannot be excluded on the basis of data obtained by the present authors. The increase of phosphorylase activity in this type of stress is ensured by several mechanisms. Moreover, the high effectivity of these hormonal factors in evoking the phosphorylase response even without major activation of the sympathicoadrenal system is underlined.
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PMID:The role played by hormonal factors in the rapid activation of liver glycogen phosphorylase in traumatized rats. 621 10

The effects of Tramadol-N2O-anaesthesia on the per- and postoperative change in blood concentrations of cortisol, prolactin, thyroxine, triiodothyronine, cyclic AMP, glucagon, antidiuretic hormone, PTH-peptide (44-68), glucose, lactate, pyruvate and free fatty acids (FFA) were investigated in connection with elective orthopaedic surgery. Anaesthesia in man with Tramadol and nitrous oxide were found to be associated with a significant elevation of plasma cortisol and plasma prolactin in man. However, cortisol secretion during anaesthesia is associated with an inhibition in T4-T3 conversion. No significant alterations in plasma glucagon concentrations were observed. Generally, surgical trauma induced a significant increase in plasma cyclic AMP with intraoperative levels between 26.4 and 34.3 pmol/ml. At the end of surgery a significant fall in plasma PTH-peptide (44-68) occurred. There was also a significant change in plasma ADH levels following induction of anaesthesia. During surgery we found plasma ADH levels up to 56 pg/ml. In addition stress and surgical trauma increased blood glucose and FFA while plasma pyruvate and plasma lactate nearly remained unchanged. The data would suggest that the non-specific stress response attributed to anaesthesia may in fact be reflecting a response to relatively light anaesthesia.
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PMID:[Endocrine reaction pattern in the course of a one-phase tramadol-N2O combination anesthesia]. 629 29


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