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)

Abnormal glucose tolerance is often found in patients with anorexia nervosa (AN). We attempted to evaluate pancreatic B-cell functioning after intravenous glucagon administration. Fourteen patients with the restricting type of AN (percentage of ideal body weight 71.5 +/- 1.6%, mean +/- SE) and 6 patients with the bulimic type of AN (77.0 +/- 3.0%) were studied. After an overnight fast, glucagon (0.02 mg/kg) was injected i.v. into all subjects and 6 normal controls. Blood samples were obtained at 0, 5, 30, 60, 90 and 120 min to measure blood glucose (BS), serum insulin (IRI) and C-peptide (CPR). The same tests were repeated in 8 patients with restricting AN after therapy and restoration of body weight (85.9 +/- 1.0% of ideal body weight). BS responses did not differ among the groups. Peak serum levels (5 min) of both IRI and CPR in restricting AN patients were significantly lower than those in bulimic AN patients and in normal controls. BS, IRI and CPR concentrations did not change significantly following restoration of body weight. Pancreatic B-cell dysfunction after glucagon administration was observed in restricting AN patients and the abnormality persisted after short-term weight restoration.
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PMID:Pancreatic B-cell functioning after intravenous glucagon administration in anorexia nervosa. 154 50

The serum ketone response to glucagon was measured in 10 patients with IDDM and 37 with NIDDM. In both groups, serum 3-hydroxybutyrate increased significantly after intravenous injection of 1 mg glucagon. The difference between the serum level of 3-hydroxybutyrate at 30 min and basal level [delta 3-OHBA(30')] was 133 +/- 25 mumol/l in the patients with IDDM, 13 +/- 8 mumol/l in those with NIDDM treated by diet alone or with oral hypoglycemic agents and 23 +/- 13 mumol/l in those with NIDDM treated with insulin. The delta 3-OHBA(30') was significantly greater in IDDM patients than in both groups of NIDDM patients (P less than 0.001). The delta 3-OHBA(30') was greater than 87 mumol/l in eighty percent of IDDM patients, but smaller than 87 mumol/l in both groups of NIDDM patients. The delta 3-OHBA(30') was correlated with the difference between the plasma level of C-peptide at 6 min and basal level [delta CPR(6')] (r = -0.540, P less than 0.001). The delta 3-OHBA(30') was not correlated with fasting plasma levels of glucose, fructosamine or hemoglobin A1c. These observations show that measurement of the serum ketone response to glucagon is a useful marker of insulin dependency. In order to determine insulin dependency, the simultaneous measurement of concentrations of ketones and C-peptide is indicated during the glucagon stimulation test.
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PMID:Serum ketone response to glucagon as a marker of insulin dependency in diabetics. 175 81

The increase in insulin requirement at the onset of adolescence is compensated by an increase of insulin secretion. This metabolic pattern persists during adolescence but is no longer present in adults. It is supposed to depend on a decrease of insulin sensitivity of uncertain origin. We compared the metabolic pattern of late adolescent girls (13-16 year old) with young women (21-30 year old) with similar body mass indexes, testing subjects with iv glucose tolerance test (IVGTT) (glucose 0.33 g/kg) and arginine test (ATT) (arginine 30 g in 30 min). In late adolescent vs adult women we observed: i) IVTT: similar k of glucose tolerance and higher insulin and C-peptide responses; ii) ATT: unmodified plasma glucose, insulin and glucagon values, higher GH plasma levels; iii) in adolescent girls GH and CPR incremental areas significantly correlated (r = 0.755, p less than 0.05). These data show that: i) the adolescent pattern of glucose metabolism persists after completion of sexual development and, ii) there is a positive correlation between GH response to arginine and beta-cell response to glucose. So GH should play a role in the impairment of glucose metabolism during adolescence.
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PMID:Glucose tolerance and insulin release in adolescent female. 176 11

Fifty obese (BMI = 40.1 +/- 1.5) subjects (21 men and 21 women; average age 38.6 +/- 3.8 years) were prescribed a 600 cal/day diet (carbohydrates 30 g, proteins 60 g, lipids 10 g). Thirty patients were also given benfluorex (three tablets/day) for six months (Group A), whereas the other 20 patients (Group B) were treated with the dietary measures only. Apart from grade II and III obesity, several patients suffered from dyslipidaemia (Group A: n = 10; Group B: n = 7), non-insulin-dependent diabetes mellitus (NIDDM) (Group A: n = 4; Group B: n = 3) or IGT (Group A: n = 8; Group B: n = 6). The usual blood and biochemical tests and clinical examinations were carried out on Days 0, 90 and 180, together with the OGTT and glucagon test to determine blood glucose levels, IRI and CPR. There was no statistical difference between the weight loss of Group A and that of Group B. In Group A there was a statistically significant reduction (p less than 0.001) in total cholesterol, triglycerides, total/HDL-cholesterol and beta/alpha-lipoproteins and a significant increase in HDL-cholesterol and alpha-lipoproteins (p less than 0.001), whereas in Group B only a significant reduction in triglycerides (p less than 0.001) was observed. In NIDDM patients treated with benfluorex, normalisation of basal blood glucose levels was accompanied by an improvement in the OGTT blood glucose curve which was statistically significant relative to Group B. Benfluorex was well tolerated by all patients and no adverse event was reported.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of benfluorex in obese patients with metabolic disorders. 259 99

In an attempt to define the pancreatic B cell function in the elderly, we subjected 88 non-obese individuals (aged between 21 and 88) to an oral glucose tolerance test (OGTT), a simple glucagon test (SGT) and OGTT-glucagon test, in which the plasma glucose, insulin and serum C-peptide (CPR) were measured. We investigated heterogeneity in glucose intolerance in the elderly and its relationship to atherosclerosis. In the OGTT and SGT test, the insulin responses (SIRI/SPG ratios) for normal, borderline and DM1 (fasting plasma glucose less than 140 mg/dl and 2 h-PG greater than or equal to 200 mg/dl) groups of the elderly (60 and above) were not significantly different from those for normal group of young and middle-aged (below 60) and were significantly higher for elderly group than for the young and middle-aged group in each glucose tolerance group. But the insulin responses for the DM2 (fasting plasma glucose greater than or equal to 140 mg/dl and 2 h-PG greater than or equal to 200 mg/dl) group of the elderly were not significantly different from those for the DM1 and DM2 groups of young and middle-aged. The insulin responses of normal, borderline and DM1 groups of the elderly with atherosclerosis were significantly higher than those of the comparable groups without atherosclerosis, while the insulin responses of the borderline and DM1 groups of the elderly with atherosclerosis were similar to those of the control group of the young. In the OGTT-glucagon test, there were no differences in the insulin response or serum CPR response among the normal, borderline and DM1 groups of the elderly, and these responses were significantly higher for the elderly group than the for young and middle-aged group in each glucose tolerance group. But these responses for the DM2 group of the elderly were not significantly different from those for the DM1 and DM2 groups of the young and middle-aged. These results indicate that the pancreatic B cell function of the normal group in the elderly remains favorable while mildly impaired glucose tolerance was exhibited by the borderline and DM1 groups, who are comparable with the normal group of the young and middle-aged. But this function was clearly reduced in the DM2 group of the elderly. These findings suggest that there is a subgroup in the elderly, which has clinically evident atherosclerosis, mild glucose intolerance and high insulin response. Their pancreatic B cell function remains favorable.
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PMID:[Pancreatic B cell function and glucose intolerance in the elderly]. 265 22

To evaluate the effect of total pancreatectomy on the secretion of human growth hormone, twenty-six patients undergoing total pancreatectomy and twelve healthy subjects (controls) were investigated. Blood glucose (BG), plasma insulin (IRI), C-peptide (CPR), immunoreactive glucagon (IRG) and human growth hormone (HGH) levels were determined. In the glucose tolerance test, the mean basal blood glucose level in the patients before operation was significantly higher than the level in the controls. The basal blood glucose level in the patients after operation was still higher than the level before operation. The responses of IRI, CPR, and IRG secretion after arginine infusion in the patients before operation were less than those in the controls. After operation, arginine infusion did not alter the levels of IRI, CPR and IRG. The mean basal HGH levels were not significantly different between the controls and the patients before and after operation. However, a statistically significant correlation was shown between the basal values of plasma HGH and those of plasma IRI in the patients after operation. Thus, it suggested that the basal secretion of HGH is closely related to the exogenous plasma insulin levels in the pancreatectomized patients. After arginine infusion, the HGH levels in the patients before operation were lower than the those in the controls, but insignificant. After operation, mean HGH levels were significantly lower than those before operation. These findings suggested the absence of pancreatic endocrine function caused by total pancreatectomy resulted in decreased responses of HGH secretion after arginine infusion.
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PMID:[Influence of total pancreatectomy on the secretion of human growth hormone and the endocrine pancreas]. 305 67

The function of the pancreatic B- and A- cell during a carbohydrate-rich meal was investigated in hyperthyroid patients, since these patients frequently present an altered handling of glucose. In basal conditions the plasma levels of glucose, immunoreactive insulin (IRI), C-peptide (CPR), proinsulin were higher in hyperthyroid patients than in normal subjects, whereas plasma glucagon was similar in the two groups. Hyperthyroid patients had high post-breakfast incremental areas of glucose and IRI and those of CPR and glucagon were normal. In post-breakfast plasma, the hyperthyroid patients had high proinsulin and normal insulin levels. The molar ratio between CPR and IRI was low throughout the test in the hyperthyroid group. In conclusion, in the hyperthyroid group the plasma levels of proinsulin were high and those of glucagon were normal; in response to the standard breakfast the levels of insulin and C-peptide were normal. These findings do not explain the altered glucose handling present in these patients.
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PMID:Plasma glucose, insulin, proinsulin, C-peptide and glucagon before and after a carbohydrate-rich meal in hyperthyroid patients. 331 63

In 20 insulin dependent diabetics and in eight age-matched healthy children, we have measured basally HbA1 and the plasma lipid profile; and both basally and after a standard breakfast of 400 cal, blood glucose, C-peptide (CPR), immunoreactive glucagon (IRG), growth hormone and nonesterified fatty acids (NEFA). No difference was found in the lipid profile of diabetic and non diabetic children. In diabetics basal blood glucose was significantly correlated to both basal C-peptide (r = 0.5332, p less than 0.05) and to the ratio C-peptide/glucagon (r = 0.8563, p less than 0.01). The C-peptide response to the breakfast was accompanied of a significant increase in IRG and NEFA in diabetics, while in non-diabetics there was no change in IRG and a significant decrease in NEFA levels. Diabetic children with basal C-peptide levels higher than 0.6 ng/ml had lower blood glucose levels (187 +/- 43 vs 315 +/- 20 mg/dl, p less than 0.02), but no difference in blood glucose or any other parameter was observed as a function of the increase in CPR after breakfast. From these results we conclude that the evaluation of residual B-cell function in diabetic children by measuring the C-peptide response to a provocative stimulus is not more informative than the single basal measurement of C-peptide and does not have an additional biological significance, at least in hyperglycaemic insulin dependent diabetic children.
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PMID:[Biological significance of the endogenous secretion of insulin in response to breakfast in diabetic children]. 332 43

In order to better understand the role of A- and B-cell function in diabetic pregnancy, we studied four groups of pregnant women at week 34-36 of gestation. Seventeen were healthy controls (C), 24 had gestational diabetes (GD), 16 had type 2 diabetes (NIDD) and 37 had type 1 diabetes (IDD). At times -20, 0, 20, 30, 45, 60, 90 and 120 min from the beginning of a 30 min infusion of 30 g of arginine intravenously, plasma glucose, glucagon (IRG) and C-peptide (CPR) were measured. Plasma glucose was higher in diabetic than in control subjects. IRG values were also higher in the GD and the NIDD women. CPR values were similar to, or slightly higher than control values in the GD and the NIDD and were much lower in the IDD women. All three variables increased during the arginine infusion in all groups, with the exception that CPR remained unchanged in the IDD. The CPR/IRG molar ratio was similar in control, GD and NIDD women; in the IDD, it was much smaller than in the other groups and was not affected by arginine. In all the diabetic patients, IRG was negatively correlated with the maternal weight gain and in the IDD IRG was positively correlated with the increase in the insulin need and with the CPR levels. In conclusion diabetes appeared to enhance the A-cell function also in pregnancy, possibly impairing the 'facilitated anabolism' and stressing the 'accelerated starvation' which are typical of normal pregnancy. Glucagon was confirmed as one possible determinant of the insulin resistance seen in diabetic pregnancy.
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PMID:Endocrine pancreatic function in insulin-dependent diabetic pregnant women. 353 67

Clinical applications of analyses of hormones in amniotic fluid (AF) have recently been increased. In diabetic pregnancy, determinations of insulin and C-peptide in AF have been suggested as good indicators of the status of the foetus. We have investigated the pancreatic alpha and beta cell function by measuring insulin (IRI), C-peptide (CPR), glucagon (IRG), somatostatin (SLI), and gastric inhibitory polypeptide (GIP) in amniotic fluid collected during basal conditions or 2 h after an arginine test in 92 diabetic and 32 non-diabetic pregnant women. During basal conditions, in diabetic pregnant women, IRI, CPR and the insulin: glucagon molar ratio (I/G) were all significantly higher while amniotic fluid-IRG was significantly lower than in the controls. After arginine stimulation, IRI increased in AF of the diabetic pregnant women but not in AF of the controls while no differences were observed in AF-GIP and AF-SLI concentrations. Higher IRI and CPR, as well as lower IRG values were significantly related to poor maternal metabolic control. The occurrence of neonatal morbidity including macrosomia was significantly associated with increased AF, IRI and CPR concentrations after an arginine challenge and these factors were the most sensitive predictors of neonatal morbidity in infants of diabetic mothers. Increased AF glucose concentrations and I/G ratios were related to neonatal hypoglycaemia; jaundice and respiratory distress syndrome were associated to low concentrations of SF-IRG.
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PMID:Gastro-entero-pancreatic hormones in amniotic fluid from normal and diabetic pregnant women. 353 68


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