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 effect of a dialysate exchange with both 1.5 and 4.25% glucose solutions on plasma levels of glucose, insulin, gastric inhibitory polypeptide (GIP), and glucagon has been investigated in 5 continuous ambulatory peritoneal dialysis (CAPD) patients. Only in the case of the 4.25% solution did plasma glucose levels rise above 100 mg/dl. 4 of the 5 patients responded to this change with a marked insulin secretion. Employing the 1.5% solution, plasma glucose remained stable and only a slight insulin stimulation was observed in 2 patients. It is concluded that provided the 4.25% dialysates are used only occasionally, there will be no continuous stimulation of the pancreatic beta-cells due to absorption of glucose from the dialysate alone during CAPD treatment. GIP levels are highly elevated in CAPD patients. A dialysate exchange with either a 1.5 or a 4.25% glucose solution had no effect on this gastrointestinal hormone. Hyperglucagonemia was also observed in this collective. An initial suppression of glucagon levels occurred in 4 of the patients after a 4.25% dialysate exchange. The 5th patient demonstrated an initial rise followed by a later decrease in glucagon, a response similar to that reported in adult onset diabetes after an oral glucose tolerance test.
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PMID:Effect of dialysate glucose load on plasma glucose and glucoregulatory hormones in CAPD patients. 388 5

The influence of Verapamil, a calcium antagonist, on circulating levels of glucose, insulin and glucagon has been evaluated in 5 normal subjects and in 5 patients with non insulin-dependent diabetes (NIDDM). An oral glucose tolerance test was performed both in basal conditions and during intravenous infusion of the drug (5 mg/h). Administration of Verapamil didn't induce any significant change on the three parameters. The small decrease of glycemia in patients affected by NIDDM and treated with Verapamil was not related to reduction of glucagonemia.
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PMID:[Effects of calcium antagonists on pancreatic endocrine secretion]. 388 22

To assess the normality of islet A- and B-cell responses to a nonglucose secretogogue as well as the modulating effect of glucose in NIDDM, we examined plasma C-peptide and glucagon responses to arginine in eight patients with NIDDM and in six age- and weight-matched nondiabetic volunteers under conditions of identical hypoglycemia (approximately 70 mg/dl), euglycemia (94 mg/dl), and hyperglycemia (approximately 190 mg/dl). Plasma C-peptide responses to glucose and to arginine in the diabetic subjects were both significantly reduced at all glucose concentrations studied (P less than 0.01-0.005). The modulating effect of glucose on both islet A- and B-cell responses (slope of relation between plasma C-peptide or glucagon response versus plasma glucose concentration) was reduced greater than 80% in the diabetic subjects (P less than 0.01). We conclude that islet A- and B-cell responses to nonglucose secretogogues are abnormal in patients with NIDDM and that this may result from a functional defect in the modulating effect of glucose on insulin and glucagon secretion, which in some patients may be compensated for by hyperglycemia.
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PMID:Abnormal glucose modulation of islet A- and B-cell responses to arginine in non-insulin-dependent diabetes mellitus. 389 67

The authors investigated the effects of clonidine (alpha-2 stimulating agent) on blood glucose, insulin and glucagon levels in order to assess the alpha-adrenergic regulation of endocrine pancreatic secretion. Ten hypertensive female subjects affected with type 2 diabetes were studied; each subject was given a protein meal (boiled beef 200 g); blood samples were taken at -30, 0, 30, 60, 90 and 120 min; after this test each subject was treated for 4 days with clonidine (0.150 mg, 3 times/day per os); at the 5th day the protein meal was repeated under the same conditions except for the added administration of clonidine. Plasma glucose, insulin and glucagon were estimated. The administration of a protein meal caused a significant increase of blood glucose (peak at 60 min), insulin (peak at 90 min) and glucagon (peak at 90 min) levels; the association of clonidine caused an increase of blood glucose (single values and total areas) without changes of insulin and glucagon levels, when compared to those obtained before clonidine treatment. In conclusion, the association of clonidine to a protein meal caused impaired glucose tolerance presumably due to a direct glycogenolytic effect, occurring in the liver on account of an alpha-2 receptor stimulation, insulin and glucagon not being involved in this phenomenon.
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PMID:Effect of clonidine on glucose, insulin and glucagon responses to a protein meal in type 2 diabetics. 389 55

As far as exaggerated arginine-induced glucagon secretion in diabetics is concerned, the authors have shown that both the restoration of blood glucose excursions and physiological insulinemia in response to arginine, obtained from an artificial endocrine pancreas (AEP) could normalize the glucagon secretory responses in diabetes mellitus. To clarify whether or not physiological glycemic excursions and/or plasma insulin profiles contribute to the normalization of the exaggerated glucagon response in diabetes mellitus, the following 4 investigations were conducted on each of 7 non-obese, non-insulin-dependent diabetic (NIDDM), and 8 insulin-dependent diabetic (IDDM) subjects, with the aid of AEP. Arginine was i.v. infused into both diabetic groups (1) in a hyperglycemic state without insulin infusion, (2) in perfect glycemic control with insulin infusion by AEP, (3) in glycemic control with AEP, but with lower plasma insulin profiles (parameters of the insulin infusion algorithm were made smaller than those of (2], (4) in a state where blood glucose levels were clamped at the same levels as obtained in (1) with the aid of glucose infusion controlled by AEP, and where physiological plasma insulin profiles were mimicked by infusing insulin at the same rates used in (2) with a pre-programmable insulin infusion system. The changes in the plasma glucagon (IRG) response in each experiment were compared with those seen in healthy subjects. For both diabetic groups it was found that: in (2) perfect normalization of glucagon response was achieved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The mechanism of exaggerated glucagon response to arginine in diabetes mellitus. 391 60

Serum C-peptide (SCPR) at fasting and after intravenous injection of glucagon was evaluated in diabetic patients with various degrees of insulin dependence, and compared with 24 h urine C-peptide (UCPR). Fasting SCPR did not differ between healthy subjects and sulfonylurea-treated patients (SU) who were considered to have definite non-insulin-dependent diabetes (NIDDM); but was significantly lower in patients with insulin-dependent diabetes (IDDM) (0.24 +/- 0.10 ng/ml in IDDM vs. 1.43 +/- 0.61 ng/ml in SU, P less than 0.001). SCPR reached a peak at 6 min after glucagon injection, except for the IDDM group. The SCPR response at 6 min after 1 mg glucagon injection was significantly lower in the SU (NIDDM) group than in the normal group (2.86 +/- 1.21 v. 4.69 +/- 1.47 ng/ml, P less than 0.001). In the IDDM group, there was no increase of SCPR after glucagon injection. Among diabetic patients, SCPR response to glucagon correlated positively to the amounts of UCPR (P less than 0.001). By analysis of the distribution patterns of SCPR response to intravenous glucagon, SCPR of 1.0 ng/ml and the increment of SCPR of 0.5 ng/ml at 6 min are to be used as cut-off points to differentiate IDDM and NIDDM. These values correspond roughly to the UCPR values below 20 micrograms/day and above 30 micrograms/day, which we previously proposed as indexes to differentiate insulin-dependent and non-insulin-dependent diabetes.
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PMID:A comparison of serum C-peptide response to intravenous glucagon, and urine C-peptide, as indexes of insulin dependence. 391 62

In a double-blind cross-over study we compared the effects of insulin plus glibenclamide, 5 mg twice daily, with insulin plus placebo during 8-week periods on metabolic parameters in 13 non-insulin dependent diabetic (NIDDM) patients poorly controlled with insulin alone. The combination therapy improved diabetic control as assessed by fasting blood glucose (p less than 0.001), 24-hour urinary glucose (p less than 0.01) and glycohemoglobin (HbA1) concentrations (p less than 0.05 at week 12). The effect tended to cease with time. Significantly higher C-peptide values were found during combination treatment than during insulin-placebo (p less than 0.01) and the changes in fasting C-peptide concentrations correlated positively with the changes in HbA1 concentrations (r = 0.56, p less than 0.05). There was no difference in glucagon concentrations, insulin binding to erythrocytes or insulin sensitivity between the two study periods. Neither did the combination therapy influence blood lipids significantly. The present study shows that the combination of insulin and glibenclamide may be of limited value in the treatment of NIDDM patients poorly controlled with insulin alone. However, thus far the long-term results are uncertain. In the absence of significant effects on insulin binding and insulin sensitivity, the improved diabetic control seems to be explained, at least partly, by glibenclamide-induced stimulation of insulin secretion.
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PMID:Transient effect of the combination of insulin and sulfonylurea (glibenclamide) on glycemic control in non-insulin dependent diabetics poorly controlled with insulin alone. 391 31

A single-blind, randomized, comparative evaluation of glyburide (GL) and chlorpropamide (CP) therapy was performed in twenty previously untreated patients with non-insulin dependent diabetes mellitus (NIDDM) of about two years duration. Only newly diagnosed patients who were never treated and whose fasting blood glucose (FBS) levels were greater than 140 mg/dl after a six to eight week trial of dietary restriction were evaluated. Metabolic studies were performed before and after four months of therapy. GL and CP produced essentially the same effects on serum levels of glucose, insulin, glucagon (IRG), growth hormone (GH), cholesterol, and triglyceride. The mean 24-hour glucose levels for both the GL and CP groups were significantly lower than the pretherapy values (p less than 0.001). The mean 24-hour insulin levels did not change significantly during therapy (p greater than 0.05). Excellent control of plasma glucose was possible during the entire day without producing nocturnal hypoglycemia. Neither GL nor CP therapy influenced the mean 24-hour levels of IRG, GH, or cholesterol. However, mean 24-hour levels of triglyceride were lower in both groups. IRG levels were elevated and the pattern of change in the insulin and IRG levels paralleled each other, which suggested that glucagon may play a role in the resistance of insulin action in NIDDM. GH levels were normal and remained unchanged during therapy. It was concluded that detailed 24-hour studies are important for better understanding the spectrum of abnormalities in newly diagnosed patients with NIDDM who were never treated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The 24-hour effects of glyburide and chlorpropamide after chronic treatment of type II diabetic patients. 392 33

In this brief review of regulatory function of gastroenteropancreatic peptides in control of intermediary metabolism in normal and diabetic states, with and without mediation by insulin and/or glucagon, a variety of possible mechanisms have been described. It is apparent that the pharmacologic actions of the peptides identified in various locations provide models for multiple routes of delivery and modes of action of effectors in this control system. Examples already exist of each of the hypothetical mechanisms illustrated in the scheme in Figure 4. It is clear that a great deal of study will be necessary in identification of the active agents and assessment of their importance in the physiology of intermediary metabolism. With respect to the possible pathophysiologic roles of regulatory peptides of the gastroenteropancreatic system other than insulin and glucagon, a number of considerations of Type I and Type II diabetes have been raised. The balance of the evidence suggests that Type I diabetes may be viewed as an insulin deficiency syndrome, so that physiological replacement with insulin may be expected to result in correction of the metabolic abnormalities. Nevertheless, the difficulty of physiologic replacement treatment, which may call for portal delivery of insulin, is well recognized, and abnormalities secondary to insulin deficiency even in "well-treated" Type I diabetes may be compounded by the effects of gastroenteropancreatic peptides other than insulin, exerted through the various mechanisms discussed. In Type II diabetes mellitus, current understanding of the pathophysiology is much less complete and no convincing description of the etiology exists. The various metabolic actions of the gastroenteropancreatic peptides, and their interactions with other endocrine, paracrine and nervous regulatory mechanisms, represent a dauntingly complex control system. The elucidation of this system can provide fertile ground for the development and testing of hypotheses for the pathophysiology of disordered metabolism in Type II diabetes mellitus.
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PMID:Insulin-mediated and non-insulin-mediated metabolic effects of gastroenteropancreatic peptides in type I and type II diabetes. 403 14

Two beta-blocking agents, non-selective propranolol and beta1-selective metoprolol, were investigated with respect to their effects on glucose metabolism in 10 hypertensive patients with non-insulin dependent diabetes mellitus (NIDDM). The patients were treated randomly for two weeks in double-blind cross-over manner with (a) propranolol, (b) metoprolol, and (c) placebo. Propranolol impaired glucose tolerance when compared to placebo. The increase in blood glucose was associated neither with changes in concentrations of serum insulin, plasma glucagon of free fatty acid nor with alterations in peripheral insulin sensitivity as measured by 125I-insulin binding to mononuclear leukocytes. Although metoprolol had no effect on blood glucose, it increased 125I-insulin binding to mononuclear leukocytes. The increase in insulin binding could contribute to blood glucose control during metoprolol treatment. In search for reasons for poor metabolic control in NIDDM, treatment with non-selective beta-blockers should be kept in mind.
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PMID:Influence of beta-blocking drugs on glucose metabolism in patients with non-insulin dependent diabetes mellitus. 612 39


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