Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma immunoreactive glucagon (IRG) was examined in volunteers with biopsy-proven cirrhosis of the liver after recovery from surgical portal--caval anastomosis. A wide range of increased total plasma IRG concentrations was found after overnight fast in groups of cirrhotic subjects with and without fasting hyperglycemia. Gel filtration chromatography of plasma showed a major component in the 3500-mol wt fraction in all cases so studied. Administration of glucose i.v. caused rapid suppression of total plasma IRG in normoglycemic and non-insulin-dependent hyperglycemic cirrhotic subjects. After administration of oral glucose, total plasma IRG was suppressed rapidly in normoglycemic cirrhotic subjects, while non-insulin-dependent hyperglycemic cirrhotic subjects exhibited delayed but prolonged suppression. Chromatography of selected plasma with glucose-suppressed total IRG showed a major decrease in the 3500-mol wt component in every case. Exaggerated increments of plasma gastric inhibitory polypeptide were demonstrable in both groups of cirrhotic individuals after administration of oral glucose, and it is speculated that this peptide may contribute to stimulation of glucagon secretion in liver disease associated with insulin deficiency.
 ...
PMID:Hyperglucagonemia in liver cirrhosis with portal-systemic venous anastomoses: responses of plasma glucagon and gastric inhibitory polypeptide to oral or intravenous glucose in cirrhotics with normal or elevated fasting plasma glucose levels. 44 82

The effects of exogenous insulin upon the response of immunoreactive glucagon (IRG) to i.v. glucose were studied in diabetic and nondiabetic subjects. In nondiabetics, a rapid injection of 25 g of glucose lowered plasma IRG levels. In adult-onset diabetics, the glucose-induced decline in IRG was normal despite a subnormal glucose-induced insulin rise, in contrast to impaired IRG suppressibility previously reported when such patients received an oral glucose load. The magnitude of their glucose-induced IRG decline was not augmented by exogenous insulin, even when insulin levels were acutely raised above 300 micro units/ml. In juvenile-type diabetics, basal IRG levels were normal following overnight insulin infusion, but the glucose-induced IRG decline was only half that of the nondiabetics. However, it became normal when hyperinsulinemia was acutely produced by supplementary insulin. Thus, whenever insulin levels rise in response to an increase in hyperglycemia, as they do spontaneously in nondiabetics and in adult-type diabetics and as they do when juvenile diabetics are given supplementary insulin together with the glucose bolus, the decline in IRG in response to an i.v. glucose load is as great as in nondiabetics. The findings are compatible with the view that glucose-induced suppression of IRG may require a concomitant rise in insulin.
 ...
PMID:Effects of insulin on the response of immunoreactive glucagon to an intravenous glucose load in human diabetes. 44 98

Bombesin acts within the brain to produce a prompt and sustained hyperglycemia, hyperglucagonemia, and relative or absolute hypoinsulinemia. Bombesin does not decrease plasma glucose turnover. Acute adrenalectomy but not hypophysectomy prevents hyperglycemia and hyperglucagonemia after intracisternal administration of bombesin. Administration of bombesin into the lateral ventricle of awake, unrestrained animals results in elevation of plasma glucose, preceded by a significant increase in plasma epinephrine and no increase in plasma norepinephrine or dopamine. Systemic administration of somatostatin prevents bombesin-induced hyperglycemia and hyperglucagonemia. These data support the conclusion that bombesin acts within the brain to increase sympathetic outflow resulting in increased adrenalmedullary epinephrine secretion, followed by depression of plasma insulin and elevation of plasma glucagon and glucose.
 ...
PMID:Central nervous system action of bombesin: mechanism to induce hyperglycemia. 46 25

We have demonstrated persistently elevated serum C-peptide concentrations in patients with chronic renal failure on chronic hemodialysis. A blunted serum C-peptide response to intravenous glucose, glucagon and tolbutamide was also found. However, the response to oral glucose stimulation was greater and more prolonged than in control subjects, probably related to the magnitude of hyperglycemia found in patients with chronic renal failure. These observations suggest the existence of a defect in the renal clearance of C-peptide although an abnormality in C-peptide secretion cannot be excluded.
 ...
PMID:Serum C-peptide in renal failure patients following stimulation of pancreatic secretion. 47 46

The effect of somatostatin (SRIF) and of insulin on the plasma levels of immunoreactive glucagon (IRG) and glucose was examined in normal (N) and depancreatized (PX) dogs. The infusion of SRIF (3 microgram/min for 15 min) caused a rapid decrease of the total IRG measured by means of an antiglucanon serum (AGS 10) which cross reacts with extracts of intestinal mucosa. This decrease was due primarily to a fall in the IRG fraction measured by an antiserum (AGS 18) specific for the carboxyl terminus of pancreatic or A-cell IRG. When the dose of SRIF was increased to 10 microgram/min for 90 min, the difference between total and A-cell IRG in the systemic blood also decreased, indicating that other IRG fractions, such as gut IRG, had also been suppressed. The introduction of 50 ml of a 5% glucose solution into a loop of ileum was followed by an increase of gut IRG measured in the regional mesenteric blood. This response was suppressed by the infusion of SRIF (3 microgram/min). Insulin suppressed the basal level of total IRG, but did not alter the gut IRG response to glucose. The SRIF- and insulin-induced reduction in plasma IRG was not associated with a reduction in plasma glucose, suggesting that the high levels of total and A-cell IRG observed in depancreatized dogs were not essential for the maintenance of hyperglycemia.
 ...
PMID:A-Cell and gut glucagon in normal and depancreatized dogs. Inhibition by somatostatin and insulin. 47 84

To define whether rapid rate of fall in blood glucose stimulates counterregulatory hormonal responses in diabetic man, blood glucose in eight hyperglycemic diabetic subjects was rapidly lowered by intravenous insulin administration. Despite precipitous declines in blood glucose, plasma epinephrine and growth hormone remained virtually unchanged. In contrast, norepinephrine and cortisol increased significantly (P less than 0.025) in the face of hyperglycemia or euglycemia, while glucagon was suppressed (P less than 0.025). A transient modest fall in mean arterial pressure and a rise in pulse rate were noted. No correlation was observed between glucose disappearance rate or decrement in glucose concentration and the hormonal responses. After sham insulin administration, no change was observed in plasma epinephrine, norepinephrine, and cortisol levels. These findings suggest that rate of fall in blood glucose per se is not a primary signal for counterregulatory hormonal response. Cortisol but not growth hormone release during falling blood glucose in diabetic subjects can occur despite elevated blood glucose levels. The etiology of norepinephrine and cortisol change is unclear.
 ...
PMID:Counterregulatory hormonal responses to rapid glucose lowering in diabetic man. 47 81

The present study provides evidence that changes in glucagon secretion are influential in determining the hyperglycemic activity of catecholamines in normal and diabetic rats. In normal fed rats, epinephrine (EPI) stimulated large increments in glucagon release and inhibited insulin secretion. In contrast, the modest hyperglycemic activity of isoproterenol (ISO) in normal fed rats correlated with its weak glucagon-releasing activity and its strong insulin-releasing activity. In alloxan-diabetic rats, the augmented hyperglycemic response to ISO was accompanied by larger increments in plasma glucagon levels than the catecholamine produced in normal fed rats. When glucagon release was inhibited by a concurrent infusion of somatostatin, the hyperglycemic responses of normal fed rats to EPI were reduced by approximately 67%. ISO-induced hyperglycemia in alloxan-diabetic rats was even more sensitive to inhibition by somatostatin since this response was reduced by approximately 90% when glucagon release was inhibited by somatostatin. These findings indicate that more than half of the hyperglycemic response to EPI in normal fed rats and nearly all of the hyperglycemia produced by ISO in diabetic rats result from increased glucagon release. Moreover, the impotence of ISO as a hyperglycemic agent in normal fed rats is probably due to insulin release which tends to suppress glucagon release.
 ...
PMID:The influence of endogenous glucagon release on hyperglycemic responses to catecholamines in normal fed and diabetic rats. 48 Jan 94

Normal subjects were infused 1) with epinephrine (50 ng/(kg.min)) for 180 min followed by epinephrine plus glucagon (3 ng/(kg.min)) for 60 min after which the epinephrine infusion rate was increased (125 ng/(kg.min)) or 2) with epinephrine plus somatostatin (500 microgram/h) for 180 min. Epinephrine increased glucose production and plasma glucagon transiently but caused persistent suppression of glucose clearance and sustained hyperglycemia (despite increased plasma insulin and gluconeogenic substrates); glucose production increased again on addition of glucagon and on increasing the epinephrine infusion rate. During epinephrine plus somatostatin, glucose production still increased transiently, but further suppression of glucose clearance caused more marked hyperglycemia. In conclusion, 1) in man hyperepinephrinemia within the physiological range caused sustained suppression of glucose clearance but only a transient increase in glucose production; 2) this transient hepatic response a) was not due to glycogen or substrate depletion, b) occurred without changes in plasma glucagon or insulin, c) was specific for epinephrine but permitted subsequent responses to changes in plasma epinephrine; 3) epinephrine can serve as a physiological regulator of glucose homeostasis in man both by increasing glucose production and by decreasing glucose clearance.
 ...
PMID:Differential effects of epinephrine on glucose production and disposal in man. 49 14

Leading physical sign of "trauma-disease" in polytraumatized patients is hypovolemic shock. Changes in metabolism have been described previously. At present there are no reports concerning the time at which these changes occur. The early posttraumatic phase is characterized by normosodiemia and initial transient hypopotassemia, which is based on the renin-angiotensin-mechanism. The metabolic acidosis depending on trauma causes decreased oxygen perfusion of tissue, which possibly is found even before alterations of circulation are detected. Already at the site of the accident hyperglycemia and hyperglucagonemia with normal values of insulin were found. The increase of blood glucose was correlated to the values of adrenalin and to the insulin antagonist glucagon. The catabolism of proteins closely related to the degree of trauma continued as long as 5 days after injury. Analysis of the blood clotting system showed that in the early phase after trauma there are changes in hemostatic potential consisting in hemostatic defect. In several essential points the early posttraumatic phase of metabolism is different from that in a later phase. These facts should be kept in mind if planning therapy.
 ...
PMID:[Metabolic changes in the multiply injured. Biochemical studies in multiply injured patients with reference to the severity of the injury]. 49 70

The present study was designed to examine the effects of intravenously injected alloxan (75 mg/kg) upon plasma somatostatin-like immunoreactivity (SLI), glucagon (IRG), insulin (IRI) and glucose levels in 6 dogs. Within 2 hours of the injection of alloxan, SLI and IRI levels decreased significantly below their respective baselines, while IRG and plasma glucose concentrations increased. At 8 hours SLI levels had increased significantly by 55 pg/ml, together with a rise in IRI and a decrease in IRG and glucose concentrations. After 24 hours, marked hyperglycemia and hyperglucagonemia had developed whereas SLI levels were not different from preinjection values.
 ...
PMID:Response of plasma somatostatin-like immunoreactivity to the administration of alloxan in dogs. 49 95


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>