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)

Pancreatojejunal anastomosis disruption still represents the main postoperative complication after pancreatoduodenectomy. In this study, a technique of occlusion of the residual pancreatic stump instead of pancreatojejunal anastomosis is proposed. Between March, 1981 and August, 1987, we performed 51 pancreatoduodenectomies, using Neoprene injection in the Wirsung duct, for carcinoma of the pancreatic head (28 cases), ampullary carcinoma (12 cases), islet cell carcinoma (5 cases), and chronic pancreatitis (6 cases). We observed a 33.3% overall morbidity, with a 5.8% operative mortality. The complications observed seemed not to be related to the technique of pancreatic stump occlusion, except for 2 pancreatic fistulas which spontaneously resolved. Abdominal ultrasound and computed tomography scan performed during the follow-up did not show any significant morphological alteration of the residual stump. Pancreatic endocrine function was assessed in 10 patients by evaluating blood glucose, plasma insulin and plasma glucagon levels both fasting and after oral glucose, and intravenous arginine infusion. These tests were performed before surgery and 15 days, 6 months, 1, 2, and 3 years after surgery. The results showed that 60% of the patients had impaired glucose tolerance before surgery and the percentage did not significantly change up to 3 years later (75%). No patient developed diabetes mellitus, and only 1 patient progressed from a normal to an impaired glucose tolerance. In conclusion, intraductal injection of Neoprene after pancreatoduodenectomy seems to be a safer procedure compared to pancreatojejunal anastomosis and does not induce a post-surgical diabetes.
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PMID:Pancreatoduodenectomy with occlusion of the residual stump by Neoprene injection. 254 44

Catecholamines acutely exert a pronounced insulin-antagonistic effect, which is mediated by beta-adrenergic receptors stimulation. Nevertheless, several patients with pheochromocytoma fail to exhibit an overt diabetic syndrome, in spite of steadily elevated plasma levels of catecholamines. This prompted us to investigate a 16 years old male patient, bearing an extra-adrenal pheochromocytoma, who displayed a slightly impaired glucose tolerance to oral glucose tolerance test, whereas fasting and post-prandial blood glucose, as well as glycaemic response to intravenous glucagon, were in the normal range. Peripheral insulin sensitivity, as evaluated by intravenous insulin tolerance test, was slightly decreased. Supine norepinephrine plasma levels were steadily upon 9 ng/ml; plasma insulin, both fasting and post-prandial, was within the normal range. beta-adrenergic receptors density of peripheral mononuclear cells was strongly reduced when compared to controls (0.97 +/- 0.08 vs 2.82 +/- 0.37 fmol/10(6) cells), without any concomitant change of affinity. Insulin binding to circulating monocytes was reduced as well (2.38 +/- 0.27 vs 5.1 +/- 0.4%/10(7) monocytes); insulin receptor affinity was quite normal (1.7 ng/ml) and total receptor number was 9,200 sites/cell. In desensitization experiments, 1 microM isoproterenol caused only a 20% decrease of beta-adrenergic receptors density in the patient's cells (70% decrease in controls). Six months after surgery, all the above modifications of receptor binding, as well as the mild glucose intolerance, were almost completely reversed. Thus, high levels of norepinephrine were able to induce a decrease of both beta-adrenoceptor and insulin receptor binding, together with a marked reduction of in vitro agonist-induced redistribution of beta-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-adrenoceptors desensitization may modulate catecholamine induced insulin resistance in human pheochromocytoma. 256 Jul 26

The effect of hyperglycemia on glucose kinetics was investigated in normal and T4-treated miniature pigs. 1. T4-treatment increased basal plasma glucose (G) (+ 20%) and glucose turnover (+36%). 2. Glucose infusion (2 mg/kg x min) in controls increased insulin and glucose utilization (Rd), but decreased glucagon and hepatic glucose production (Ra). After T4-treatment glucose increased insulin, decreased glucagon and Ra but only a slight effect on G and Rd were observed. 3. Infusing glucose + somatostatin resulted in hyperglycemia in both groups due to an initial fall in Ra and Rd followed by an increase in Rd, where total Ra (endogenous + exogenous exceeded Rd. Glucose intolerance was more pronounced in controls, due to a T4-induced increase in Rd. During this non-steady state the increment in Rd per increment in G was calculated and showed 1.5 in controls and 2.5 after T4-treatment. These data give evidence that thyroid hormones increase glucose utilization during hypoinsulinemia.
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PMID:Glucoregulatory function of thyroid hormones: evidence for an insulin-independent effect. 257 Jul 10

To evaluate the influence of an infective agent, severity of infection and the age of the patient on infection-induced glucose intolerance, concentrations of fasting blood glucose, serum insulin (n = 31) and plasma glucagon (n = 22) were measured and the oral glucose tolerance test (OGTT) was carried out (n = 26) during acute and convalescence phases and after complete recovery in patients with viral (n = 17) or bacterial (n = 14) infections. Serum insulin was increased (P less than 0.001) but plasma glucagon was decreased (P less than 0.01) both during acute infection and the convalescence period. In the acute stage, 2-h values of blood glucose (P less than 0.01) and serum insulin concentrations (P less than 0.001) during OGTT were elevated. The index of insulin resistance (glucose x insulin) was increased by 33% during infection and by 28% during convalescence (P less than 0.001). The observed changes did not correlate with the severity of infection, were more pronounced in younger patients than in older ones and were not dependent on the infective agent. It is clinically important to recognize that the restoration of insulin sensitivity takes longer than the immediate recovery period from the infection.
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PMID:Glucose intolerance in acute infections. 264 79

When tested in insulin-deficient animal models of diabetes, islet activating protein (IAP) has been shown to increase the secretion of insulin and to improve glucose intolerance. The genetically obese fa/fa rat is an animal model of impaired oral glucose tolerance that does not have reduced insulin secretion. In this model IAP treatment increases basal insulin levels, resulting in lower basal glycemia. However, glucose tolerance following an oral glucose load was worsened by IAP. This was found to be due to an exaggerated stimulation of hepatic glucose production (HGP) following glucose, a defect that is already present in the absence of IAP. IAP has been reported to inhibit (by ADP ribosylation) the inhibitory regulatory protein (Ni) of adenylate cyclase. It is therefore suggested that the increased HGP following oral glucose in fa/fa rats either in the absence or in the presence of IAP treatment may result from a cAMP-mediated mechanism. A beta adrenergic activation or a stimulation of glucagon output could therefore be potential candidates responsible for glucose intolerance in obese fa/fa rats.
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PMID:The effects of islet activating protein on oral glucose tolerance in the genetically obese fa/fa rat. 265 21

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

The effect of burn injury on blood sugar levels, serum insulin levels and glucose tolerance was studied in male rats. In the burned group (following 50 per cent surface burn injury), the blood sugar level was significantly increased after burn injury in comparison with control uninjured rats. Hyperglycaemia was blocked by injection of phentolamine (10 mg/kg) for 24 h or propranolol (50 micrograms/kg) 30 min before burn or if the animals were adrenalectomized 4 days before injury. Serum insulin levels were significantly decreased in the scalded rats and their glucose tolerance was impaired. Early hyperglycaemia probably arises as a result of adrenal medullary hyperactivity. The initial rise in blood glucose probably arises from glycogen breakdown, followed later by increased hepatic production of glucose. The 50 per cent body surface scald injury is followed, acutely, by a period of glucose intolerance. In part, this intolerance may be due to decreased serum levels of insulin. The inadequate response of insulin secretion in response to glucose loading may be due to inhibition of insulin secretion by pancreatic beta cells caused by elevated catecholamine levels, possibly in combination with the action of antagonists such as glucagon, which may be secreted in excess as a result of stimulation by catecholamines.
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PMID:Hyperglycaemia after burn injury. 266 59

Hyperinsulinemia and impaired glucose tolerance are associated with liver cirrhosis. To investigate whether insulin-degrading activity in liver tissue plays a role in hyperinsulinemia, we assayed this activity in biopsy tissue from healthy and cirrhotic subjects. There was no difference in insulin degradation between these two groups. Also glucagon-degrading activity in liver tissue, which is catalyzed by the same enzyme as insulin-degrading activity, did not differ between the two groups studied. Therefore, insulin-degrading activity does not appear to be involved in the hyperinsulinemia that occurs in liver cirrhosis. The study provides indirect evidence that hyperinsulinemia and impaired glucose metabolism in liver cirrhosis are due to different mechanisms (receptorial and post-receptorial defects, and altered feedback inhibition of insulin secretion).
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PMID:Insulin and glucagon degradation in liver are not affected by hepatic cirrhosis. 268 Jan 68

A standard oral glucose tolerance test was performed in 86 healthy premenopausal obese Arab women (BMI greater than or equal to 30) Glucose, insulin and glucagon were measured at 0, 30, 60, 90 and 120 min. Sex hormone binding globulin (SHBG), plasma lipids and uric acid were also estimated. Waist-hip circumference ratio (WHR) had significant positive correlation with age, triglycerides (TG), uric acid, fasting and 120 min glucose, and 120 min insulin and significant negative correlation with SHBG. Body mass index (BMI) had significant correlation with uric acid, fasting and 120 min insulin, and significant negative correlation with high density lipoprotein cholesterol (HDL Chol). When separated in two subgroups, with WHR greater than 0.80 (41), and less than or equal to 0.80 (45 cases), plasma glucose was in the diabetic range in seven; and impaired glucose tolerance (IGT) in 11 women in the former subgroup. Only three with IGT but no diabetics, were in lower WHR subgroup. WHR in diabetics (0.93), and in IGT cases (0.90) was significantly higher than in other women (0.80). Fasting insulin was not different, but at 90 and 120 min, insulin was higher in the high WHR subgroup who had also higher fasting, 90 and 120 min glucose. Glucagon level, though slightly higher in the higher (WHR) subgroup, may indicate relative hyperglucagonaemia because of the associated significantly higher glucose. Compared with age matched non-obese controls, obese women in both subgroups had significantly higher insulin, uric acid and significantly lower HDL Chol and lower glucagon (insignificant). Obese women in the higher WHR subgroup (greater than 0.80) had also significantly higher systolic blood pressure, TG and lower SHBG.
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PMID:Pattern of obesity and insulin, glucagon, sex hormone binding globulin and lipids in obese Arab women. 269 44

In diabetes-prone BB rats, 30 to 50% of animals undergo autoimmune destruction of the pancreatic B-cells leading to a short period of glucose intolerance, followed by an abrupt onset of diabetes. We have examined whether the glucose intolerance period and the onset of diabetes are associated with changes in insulin sensitivity, using the euglycaemic hyperinsulinaemic clamp coupled with [3-3H] glucose infusion. Glucose intolerant rats were detected by a transient glycosuria one hour after an oral glucose load performed every four days. Insulin sensitivity studied in these rats the day following their detection was normal. Other diabetes-prone BB rats were tested daily and studied on the first day of glycosuria. In the basal state, glucose production was increased in diabetic rats (11.3 +/- 1.1 vs 7.1 +/- 0.8 mg.min-1.kg-1, p less than 0.05). Tissue glucose utilization was similar in diabetic and control rats (8.3 +/- 0.5 vs 7.1 +/- 0.8 mg.min-1.kg-1) despite a three fold higher glycaemia in the diabetic rats. During the hyperinsulinaemic clamps, glycaemia was clamped at 6.1-6.6 mmol/l in diabetic and control rats. A decreased insulin sensitivity was observed in diabetic rats at submaximal (200 microU/ml) and maximal (1500 microU/ml) insulin concentrations for both inhibition of hepatic glucose production and stimulation of glucose utilization. No autoantibodies against insulin could be detected in the plasma of diabetic rats. Plasma concentrations of glucagon, catecholamines, ketone bodies and fatty acids were similar in control and diabetic rats during the clamp studies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Normal insulin sensitivity during the phase of glucose intolerance but insulin resistance at the onset of diabetes in the spontaneously diabetic BB rat. 269 64


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