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)

Clinical and biochemical variables were examined during two standardized, low-dose insulin regimens in seven subjects with diabetic ketoacidosis and one with hyperosmolar coma, in order to determine whether glucagon levels can be suppressed in ketoacidosis and whether hyperglucagonaemia influences the clinical and biochemical responses to treatment. Glucagon concentrations were significantly elevated (36.6-697.0 pmol/l) at presentation in all subjects. After institution of insulin treatment (4-8 u/h), glucose and glucagon levels decreased rapidly, and in five of the eight subjects glucagon levels reached undetectable concentrations (less than 3.0 pmol/l) during the initial treatment period. Further, neither plasma glucagon concentrations at presentation, nor the rate of glucagon decline during insulin treatment, appeared to influence the rapidity of the glucose decline or the persistence of the ketoacidosis. Thus, low-dose exogenous insulin suppresses glucagon secretion in diabetic ketoacidosis, and the changes in glucagon concentrations during treatment are unrelated to the clinical response.
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PMID:Glucagon and diabetes. I. The failure of hyperglucagonaemia to influence the response of established diabetic ketoacidosis to therapy. 40 39

Alterations in insulin and glucagon levels might account for the plasma amino acid imbalance of cirrhotics. In order to verify this hypothesis we evaluated basal insulin, glucagon, branched-chain amino acids, aromatic amino acids, and free tryptophan in 13 controls and 37 cirrhotics divided on the basis of their mental state; in 4 patients the hormonal and amino acid patterns were sequentially studied during various stages of encephalopathy. Glucagon is high in cirrhotics and progressively increases with the worsening of the mental state. Free tryptophan and aromatic amino acids show a similar behavior and significantly correlate with glucagon levels (r = 0.67 and r = 0.81, respectively). On the other hand insulin levels, which are high in cirrhotics without encephalopathy, fall in the presence of deep coma. Insulin did not correlate with any of the plasma amino acids considered. Our data suggest that the catabolic state associated with increased glucagon levels may account for some of the alterations in the plasma amino acid profiles of cirrhotics. Portal-systemic shunting does not seem to be the common cause of both hyperglucagonemia and hyperaminoacidemia. Decreased branched-chain amino acid levels may be related to factors different from those involved in the alterations of carbohydrate homeostasis.
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PMID:Insulin and glucagon levels in liver cirrhosis. Relationship with plasma amino acid imbalance of chronic hepatic encephalopathy. 46 10

Glucagon is secreted not only by A2-cells of the pancreatic islets but also by A cells in the gastric fundus and duodenum. Several reports have demonstrated that the glucagon plasma concentration is increased in genetic diabetes as well as in many conditions associated with a decreased glucose tolerance such as hepatic cirrhosis, myocardial infarction, infectious diseases, burns, taumatic shock, glucagonomas, acute pancreatitis, acromegaly, pheochromacytoma and Cushing's syndrome. Hyperglucagonemia is particularly important in diabetic ketoacidosis and in non-ketotic hyperosmolar coma. The mechanisms responsible for the diabetic's hyperglucagonemia remain controversial. According to several authors, the increased glucagon secretion is, for its main part, secondary to a prolonged defect in insulin secretion and thus relatively insensitive to an acute insulin administration. According to others, the A cell abnormality is of primary origin, independant from insulin deficiency and its effects are cumulative with those of the insulin lack. Several reports dealing with induced or spontaneous experimental diabetes are in favor of the first or the second hypothesis. It appears likely that glucagon plays a role in the metabolic derangments of diabetes. Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. These results illustrate the contribution of glucagon in the pathogenesis of hyperglycemia and ketosis. Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Although controversial, the role of glucagon in ketogenesis appears likely.
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PMID:[The role of glucagon in hyperglycemia. A review (author's transl)]. 79 28

The growth-hormone-release-inhibiting hormone somatostatin was infused in seven juvenile diabetic subjects during an arginine infusion test and in six juvenile diabetic subjects during an L-dopa stimulation test. The plasma growth hormone response to arginine and L-dopa was completely inhibited by somatostatin. The plasma pancreatic glucagon response to arginine was also inhibited by somatostatin. The plasma pancreatic glucagon level was not changed by L-dopa, but somatostatin induced a significant fall in this level. The plasma glucose increase after arginine and L-dopa administration was slightly inhibited by somatostatin. The arginine-induced fall in free fatty acids was prevented by somatostatin, and the L-dopa-induced rise in free fatty acids was enhanced by somatostatin. The growth hormone- and glucagon-surppressive effect of somatostatin may prove useful in controlling the metabolic state and in preventing the development of angiopathy in diabetic patients. A somatostatin preparation with prolonged activity is needed for lifelong administration, but the presently available compound may be of value as an adjunct in the standard treatment of diabetic ketoacidosis and coma.
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PMID:The effect of somatostatin on the rise of growth hormone and glucagon secretion induced by arginine and L-dopa in diabetic patients. 115 17

Serial basal blood glucose, serum insulin, cortisol, growth hormone, glucagon and catecholamine examinations were performed in 81 brain-injured patients. 32 patients with severe injuries of other parts of the body (chest, abdomen, limbs or polytrauma), and 17 patients with non-traumatic acute brain lesions served as double control. In the brain-injured patients there is a close relation between changes of the state of consciousness and those of basal blood glucose levels: the deeper coma the higher and wider is the pathological glucose-level range. Four types of blood-glucose changes could be identified in the background of which different alterations of each hormone level were observed. Fatal outcome could be predicted in a non-diabetic patient in the first days when seeing: 1) Fasting hyperglycaemia above 14 mmol/l; 2) Fluctuating basal blood glucose levels between 5 and 22 mmol/l; 3) Deeply depressed and unchanged basal insulin level; 4) Extremely high cortisol level; 5) Decreased plasma epinephrine level. These changes in the carbohydrate metabolism seen after acute brain lesions are not identical to diabetes mellitus.
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PMID:Significance of endocrine studies in the general assessment and prediction of fatal outcome in head injury. 141 38

After vagal collapsus, hypoglycemia is the emergency most often seen in the dental office. It usually happens among the treated diabetic population; there are approximately one million diabetics in France. Its sudden appearance requires an emergency treatment with oral or IV intake of glucose, or the injection of glucagon. Hypoglycemia is defined by a drop of the blood glucose level below the normal values. Of sudden onset, the clinical signs of hypoglycemia can vary, specially the neurological and psychiatric manifestations, and they can lead to a coma. The objective diagnosis relies on the blood glucose level.
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PMID:[Hypoglycemia]. 181 6

We have seen a case of "diabetic non-ketotic hyperosmolar coma" with ketosis. An 84-year-old man was brought into the hospital in a deeply comatous and dehydrated state. The initial blood glucose level was 1252 mg/dl with plasma osmolarity of 435 mOsm/l, but no ketonuria was detected by the nitroprusside method (Ketostix). However, the plasma 3-hydroxybutyrate (3-OHBA) level was 5 mM in a newly developed bedside film test. The serum ketone bodies were later found to be 5.56 and 0.82 mmol/l for 3-OHBA and acetoacetate (AcAc), respectively. A marked increase in glucagon, cortisol and ADH with renal dysfunction (creatinine 5.0 mg/dl) were noted. An abnormal electrocardiogram, occular convergence and chorea like movement disappeared after correction of metabolic disturbances. The moderate level of IRI (14 microU/ml) on admission and a good response to glucagon 2 months after admission also indicate that the present case is a typical hyperosmolar non-ketotic coma. Because of a preferential increase in 3-OHBA, ketonuria seemed to be absent in the regular nitroprusside test. Marked dehydration is thought to cause renal dysfunction, and the increase in ADH may have helped to prevent further aggravation of ketoacidosis. We propose to change the term hyperosmolar non-ketotic coma (HNC) to diabetic hyperosmolar coma (DHC), because sometimes patients with hyperosmolar non-ketotic diabetic coma are ketotic, as seen in the present case. Determination of 3-OHBA or individual ketone bodies in blood is important and essential for the differential diagnosis of diabetic coma. The diagnosis of either ketoacidotic or hyperosmolar coma should be made depending on the major expression of ketoacidosis or hyperglycemic hyperosmolarity.
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PMID:A case of diabetic non-ketotic hyperosmolar coma with an increase with plasma 3-hydroxybutyrate. 184 65

A randomised controlled trial of insulin and glucagon infusion was carried out in 18 patients in grade III or IV coma from fulminant hepatic failure due to viral or drug-induced hepatic necrosis to see whether mortality could be reduced by stimulating hepatic regeneration. Nine patients received a continuous infusion of insulin 3 U/h and glucagon 200 micrograms/h made up in 5% dextrose containing 1% human albumin solution (HAS) while controls received 5% dextrose and HAS alone. Baseline plasma insulin and glucagon levels were comparably raised in both groups and, on infusion, rose significantly higher in the insulin- and glucagon-treated patients compared to controls. Two control and one treated patient recovered. Median survival time from enrolment to death was similar for insulin- and glucagon-treated patients and controls--2 and 3 days, respectively. Insulin and glucagon therapy did not enhance hepatic synthetic function, as measured by a fall in prothrombin time or a rise in alpha-fetoprotein; nor did it stimulate hepatic regeneration, only one patient in each group showed histological evidence of hepatic regeneration at post-mortem.
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PMID:Failure of insulin and glucagon infusion to stimulate liver regeneration in fulminant hepatic failure. 219 8

One hundred and fifty-eight patients with insulin dependent diabetes mellitus attending two Auckland outpatient clinics answered a questionnaire about hypoglycaemia. Almost all (98%) had experienced hypoglycaemic episodes and for 30% these were a major problem. Seventy-seven percent reported nocturnal hypoglycaemia, 39% of whom required external assistance during episodes. Forty-three percent had experienced coma, or convulsions during hypoglycaemia and a small group, 7%, had recurrent severe episodes. Twenty percent carried no diabetic identification and 13% did not routinely carry a glucose supply. Only 38% of patients kept glucagon at home. Forty percent of patients driving vehicles had experienced hypoglycaemia while driving and 13% reported traffic accidents attributed to hypoglycaemia. Hypoglycaemia is a major problem for many patients taking insulin. Improved education, wider availability of glucagon and more liberal glycaemic control of patients with problematic hypoglycaemia may be advisable.
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PMID:Hypoglycaemia in insulin dependent diabetic patients attending an outpatients' clinic. 237 62

Severe hypoglycemic episodes in diabetic children are a serious complication of present medical therapy. With the recent trend towards intensified insulin therapy, the incidence of severe hypoglycemia will probably increase. The pathophysiological mechanisms in the development of severe hypoglycemia are lack of modulation of plasma insulin levels, diminished or abolished glucagon release, delayed epinephrine release, and diminished glucose threshold for awareness of hypoglycemic symptoms, especially in well stabilized diabetics. The consequences of severe hypoglycemia are EEG changes, focal or generalized convulsions, (rarely) partial or generalized epilepsy, and disturbances of cognitive function probably due to neuronal damage. Some of the risk factors can easily be understood and are preventable. A highly increased risk factor is a low HbA1, and a complete lack of endogenous insulin secretion. However, in our experience human insulin is not an additional risk factor. Home blood glucose monitoring for determining the correct insulin dose and food supply is of great prophylactic importance. In the presence of coma in a diabetic child due to hypoglycemia, i.m. glucagon or i.v. glucose should be administered immediately in the correct dose. Following a severe hypoglycemic episode the glucose equilibration should be somewhat less strict. Regular education of the patient on risk factors, prevention and therapy of hypoglycemia is of great importance.
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PMID:[Hypoglycemia in childhood diabetes]. 240 80


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