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 physiological control of muscle protein balance has been reviewed. In addition to trauma, fasting and reduced activity have been shown to cause muscle protein loss through changes in synthesis and breakdown. Many of the effects of these states are mediated by alterations in the concentrations of insulin, glucagon, steroids and catecholamines. Branched-chain amino acids also appear to have specific effects in improving protein synthesis. Recently, prostaglandins have been identified as having a central role as mediators in the control of protein metabolism by many hormones and pathological states. Identification of factors which control muscle protein synthesis leads to the possibility that the metabolic response to illness and injury and its attendant muscle protein loss could be open to pharmacological manipulation. Inhibition of prostaglandin synthesis by non-steroidal anti-inflammatory drugs can improve muscle protein turnover, but their clinical usefulness may be limited by side-effects. Hormonal manipulation may offer the possibility of abolishing the metabolic response. For example, inhibition of adrenal secretion in surgical patients by spinal anaesthesia appears to modify many of the metabolic effects of injury. A variety of other treatments have been used to minimize the metabolic derangements of injury. Some of these have considerable potential, but as yet clinical benefits from their use have not been positively identified. It is likely that a pharmacological approach to the nutritional disorders of stress and injury will prove to be of major interest in the future.
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PMID:Regulation of muscle protein turnover: possible implications for modifying the responses to trauma and nutrient intake. 314 8

We have compared two groups of patients given low- or high-dose fentanyl anaesthesia. Arterial blood samples were collected for measurement of glucose, free fatty acids (FFA), glycerol, beta-hydroxy-butyrate, insulin, c-peptide, glucagon, human growth hormone (HGH), cortisol and adrenaline concentrations. After induction of anaesthesia, blood concentrations of most of these substances decreased. After the start of surgery the concentrations of cortisol, glucose, HGH, FFA and beta-hydroxy-butyrate increased significantly in the group anaesthetized with the lower dose of fentanyl. In the group that received high-dose fentanyl anaesthesia the plasma concentrations of almost all the hormones and substances measured remained relatively low. The differences between the two groups during surgery were significant for adrenaline (P less than 0.001) and cortisol (P less than 0.001). High-dose fentanyl appears to block the trauma-induced stress response seen in patients anaesthetized with low dose fentanyl.
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PMID:High- and low-dose fentanyl anaesthesia: hormonal and metabolic responses during cholecystectomy. 320 28

The standard value of serum insulin was determined to be less than 75 microU/ml with ninety-eight female adult cynomolgus monkeys of wild origin. Then, fifteen apparently healthy laboratory-bred female cynomolgus monkeys aged 6-8 years were studied to know the usefulness of the arginine tolerance test (ATT) by measuring blood glucose, insulin and glucagon. Prior to ATT, all animals had been diagnosed as non-diabetic by the intravenous glucose tolerance test (IVGTT). Arginine hydrochloride was infused intravenously at a dose of 0.5 g/kg. BW under anesthesia. According to the standard value of insulin, fifteen animals were divided into two groups, that is, the low (n = 7) and the high (n = 8) value groups. In the low value group, glucose and insulin value did not change significantly after arginine infusion and their responses were similar to those in the control group (saline infused, n = 4). But glucagon markedly increased from 10 to 45 minutes post infusion. In the high value group, glucagon response was similar to that in the low value group, while glucose and insulin values significantly decreased. It is concluded that the pancreatic alpha-cell function (glucagon secretion) can be judged by the ATT in the cynomolgus monkey but the beta-cell function (insulin secretion) can not be diagnosed.
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PMID:[Serum insulin concentration and arginine tolerance test in the cynomolgus monkey (Macaca fascicularis)]. 328 55

The influence of the upper abdominal autonomic denervation on the secretions of insulin (IRI), vasoactive intestinal polypeptide (VIP), secretin, pancreatic glucagon (IRG) and gut glucagon-like immunoreactivity (Gut GLI) was studied. Adult mongrel dogs, which were divided into control, truncal vagotomy and upper abdominal autonomic denervation groups, were investigated by intraduodenal glucose infusion test under general anesthesia. The glucose level and the response of insulin, VIP, secretin, IRG and Gut GLI secretions in the truncal vagotomy group showed no significant difference compared with those in the control group. These findings suggested that the vagus nerve is not concerned largely in the glucose level and in response of insulin VIP, secretin, IRG, and Gut GLI induced by intraduodenal glucose loading. In the upper abdominal denervation group, severe diarrhea was manifested within 60 minutes after the intraduodenal glucose infusion test, and significantly increased responses were shown in secretions of insulin, VIP, secretin, IRG, and Gut GLI. These findings suggested that upper abdominal autonomic denervation acted acceleratory on the secretions of insulin, VIP, secretin, IRG and Gut GLI by intraduodenal glucose infusion test. In addition, it was suggested that dissection of upper abdominal autonomic plexus caused diarrhea after the intraduodenal glucose infusion test.
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PMID:[Influence of upper abdominal autonomic denervation on pancreatic and gut hormone secretion]. 343 38

Using adult mongrel dogs, pyloric motor activity and gastric emptying observed by phototransducer (P.T.) under anesthesia and by strain gage transducer (S.G.T.) under consciousness. Pyloric motor activity and function were investigated in the dogs with distorted pylorus after instorations of Daclon tube, pyloric resection and pyloric stenosis. The pyloric sphincter responses to gastrin, pancreozymin, secretin, glucagon, atropine, morphine, naloxone and enkephalin administrated intravenously were observed. Gastroduodenal motor activity in relation to the changes of gastrointestinal hormone levels were measured before and after truncal vagotomy (TV) and selective proximal vagotomy (SPV) with or without pyloroplasty. Results are summarized as follows; 1. The pyloric motility recorded by P.T. was well correlated with the contractile activity recorded by S.G.T. under the anesthesia, although the pylorus was never completely closed and showed tonic movements. 2. The pyloric motor activity under the consciousness was different from gastric and duodenal motor activity. 3. After SPV, the gastrin responses to the test meals were significantly increased so that the pyloric motility was disturbed. The fact mentioned above, the pyloric functional disorder after the SPV was partly due to the hypergastrinemia. Pyloroplasty for the SPV inhibited the serum gastrin level. It was suggested that the pyloroplasty for the SPV was necessary to prevent possible hypergastrinemia after SPV.
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PMID:[Pyloric motor activity and function with special reference to pyloroplasty after vagotomy]. 344 57

Since hypothermia is commonly used to lower local and general metabolism during cardiopulmonary bypass, we attempted to identify its specific effects on glucose-insulin interactions. A group of nondiabetic patients undergoing hypothermic (28 degrees C) cardiopulmonary bypass with ischemic (cold) cardiac arrest was compared to a similar group operated on under normothermic conditions with potassium cardioplegia. In the absence of exogenous dextrose administration, hypothermia blocked insulin secretion for the duration of the operation. It also inhibited insulin secretion in response to an exogenous dextrose load (e.g., the priming fluid of the cardiopulmonary bypass circuit) or a glucagon injection, but this inhibition was lifted by rewarming. Blood glucose levels, which during normothermia were mildly elevated even in the absence of dextrose administration, remained normal during the hypothermic phase of cardiopulmonary bypass. By the end of the rewarming period, however, blood glucose levels had reached the same level as observed under normothermic bypass, a fact suggesting that the cold inhibition of hepatic glucose production had been only temporary. Cold inhibition of hepatic glucose production also explains why glucose clearance after a sudden dextrose load was initially faster at low body temperature than at normal temperature. Glucose-clamp studies indicated that insulin resistance was initiated by anesthesia and surgical trauma, and further accentuated by cardiopulmonary bypass, in association with elevated levels of hormones indicative of surgical stress. Regardless of body temperature changes, the assimilation of glucose by nondiabetic subjects during and immediately after bypass called for the infusion of large doses of insulin. A comparison with diabetic subjects showed that insulin-dependent patients (type I diabetes) required no more insulin during cardiopulmonary bypass than normal subjects, whereas patients with type II diabetes exhibited a marked insulin resistance during the operation and in the immediate postoperative period.
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PMID:Glucose-insulin interactions during cardiopulmonary bypass. Hypothermia versus normothermia. 351 20

In an attempt to know the role of the pineal gland on glucose homeostasis, the blood plasma concentrations of glucose, insulin and glucagon under basal conditions or after the administration of nutrients were studied in the jugular vein of conscious pinealectomized (Pn), melatonin-treated pinealectomized (Pn + Mel) and control (C) rats. Glucose levels were smaller in C than in Pn rats, while immunoreactive insulin (IRI) concentrations were significantly greater in C than in Pn rats. Contrary to this, immunoreactive glucagon (IRG) levels were significantly greater in Pn than in C animals. Melatonin treatment of Pn rats induces an increase of IRI concentrations and a reduction in IRG levels. Similar changes were obtained when hormonal determinations were carried out in portal blood plasma. Although ether anesthesia increases circulating glucagon levels in the porta and cava veins, the qualitative changes of plasma insulin and glucagon in Pn and Pn + Mel were similar to those found in conscious rats. To determine the effects of nutrients on pancreatic hormone release, intravenous arginine or oral glucose were administered to the animals of the three experimental groups. In C rats, both glucose and IRI levels reached a peak 30 minutes after glucose ingestion, decreasing thereafter. However, in Pn rats a glucose intolerance was observed, with maximum glucose and insulin concentrations at 60 minutes, while in Pn + Mel animals, glucose and IRI concentrations were in between the data obtained with the other two groups. Furthermore, glucose ingestion induced a significant reduction of IRG levels in all the groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of pinealectomy on plasma glucose, insulin and glucagon levels in the rat. 351 10

This study was undertaken to determine the effects of pentobarbital anesthesia (50 mg/kg ip) on glucose kinetics and individual tissue glucose utilization in vivo, in chronically catheterized rats. Glucose turnover studies were carried out using [3-3H]glucose as tracer. A transient hyperglycemia and an increased glucose production were observed 3 min after induction of anesthesia. However, 40 min after induction of anesthesia, glycemia returned to the level observed in awake animals, whereas glucose turnover was decreased by 30% as compared with unanesthetized rats. These results are discussed with regard to the variations observed in plasma insulin, glucagon, and catecholamine levels. Glucose utilization by individual tissues was studied by the 2-[1-3H]deoxyglucose technique. A four- to fivefold decrease in glucose utilization was observed in postural muscles (soleus and adductor longus), while in other nonpostural muscles (epitrochlearis, tibialis anterior, extensor digitorum longus, and diaphragm) and other tissues (white and brown adipose tissues) anesthesia did not modify the rate of glucose utilization. A decrease in glucose utilization was also observed in the brain.
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PMID:Effect of anesthesia on glucose production and utilization in rats. 354 31

The present study was performed on eight young pigs to test the hypothesis that glucagon increases hepatic oxygen supply to a greater extent than hepatic oxygen uptake, providing a better hepatic oxygen supply-demand relationship. The experiments were performed under pentobarbital sodium anesthesia and controlled ventilation. Splanchnic blood flow was studied using radioactive microspheres. Glucagon was administered in doses of 1 and 5 micrograms X kg-1 X min-1. During glucagon infusion, hepatic arterial blood flow substantially increased, splenic and pancreatic blood flows increased moderately, while stomach and intestinal blood flows, as well as portal blood flow did not change significantly. Shunting of both 9- and 15-micron spheres through preportal tissues did not change significantly. Oxygen content in arterial or portal venous blood did not change significantly, while it increased in hepatic venous blood by 30%. There were no differences in the effects between the doses of glucagon administered. There was no correlation found between changes in hepatic oxygen supply and cardiac output or blood pressure. The changes observed during glucagon administration resulted in an increase in oxygen delivery to the liver and hepatic oxygen supply-uptake ratio.
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PMID:Glucagon increases hepatic oxygen supply-demand ratio in pigs. 357 24

To examine the effects of postoperative epidural analgesia with local anaesthetics or morphine on the excess nitrogen loss after upper abdominal surgery and to assess the roles of catabolic hormones in the nitrogen loss, urinary excretion of nitrogen and catecholamines and plasma concentrations of cortisol and glucagon were measured in three groups of patients undergoing elective gastrectomy. Group G patients received the operation under general anaesthesia, and their postoperative pain was relieved by intermittent injections of analgesics. Group PE received prolonged epidural analgesia with local anaesthetics during and after surgery. Group EM received epidural analgesia intra-operatively and epidural morphine postoperatively. Urinary nitrogen excretion during the first three postoperative days was significantly less in the PE and EM groups than in the G group, and the PE group excreted slightly less nitrogen than the EM group. In the G group, urinary excretion of adrenaline increased mainly on the day of operation, and noradrenaline chiefly on postoperative days. These catecholamine responses were almost completely abolished in the PE group, and significantly inhibited in the EM group. Plasma cortisol response was most remarkable shortly after the operation and then decreased in all groups, but was significantly lower in the two epidural groups than in the G group throughout the study. Plasma glucagon increased postoperatively in all groups, and the increase was less pronounced in both epidural groups than in the G group. These results suggested that an elevated sympathetic activity, represented by increased noradrenaline excretion and elicited by painful nociceptive and sympathetic nervous afferents, is responsible for the postoperative nitrogen loss which is mediated by glucagon and cortisol.
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PMID:Effects of epidural administration of local anaesthetics or morphine on postoperative nitrogen loss and catabolic hormones. 359 44


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