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)

Eight insulin-dependent non pregnant (IDD-NP), 10 insulin-dependent pregnant (IDD-P) and 9 pregnant control women were studied. During intravenous arginine challenge (ATT) there were lower glucose and higher glucagon plasma levels in the IDD-P when compared to the IDD-NP. IRG levels in response to ATT were also significantly higher in diabetic than in non diabetic control pregnant women. These results seem to indicate that pregnancy in diabetic women, in contrast to that observed in normal women, enhances glucagon secretion with impairment of the physiological mechanism of the facilitated anabolism present in normal pregnancy.
Acta Diabetol Lat
PMID:Influence of pregnancy on glucagon levels in insulin-dependent diabetic women. 39 52

Preserving pancreatic islets for 7 days by a making use of the organ culture, we studied the insulin-releasing activity at the time of administration of glucose and various digestive tract hormones for the purpose of clarifying the function of preserved pancreatic islets. Furthermore, we transplanted pancreatic islets preserved for 3 to 5 days into the portal vein of rats with streptozotocin-induced diabetes and reached the following conclusions: (1). The islets of Langerhans of the pancreas responded well to glucose up to the seventh day of preservation and showed patterns similar to those of fresh pancreatic islets with respect to both the dose response and the time response. (2). Preserved pancreatic islets of the pancreas had insulin-releasing activity almost equal to that of fresh pancreatic islets against stimulation by glucagon, tolbutamide, and various digestive tract hormones. (3). Rats with streptozotocin-induced diabetes showed a marked improvement in blood glucose and urine glucose following transplantation of preserved pancreatic islets into the portal vein, and this effectiveness persisted for 6 to 8 weeks.
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PMID:Insulin-releasing activity and successful transplantation of pancreatic islets preserved by tissue culture. 41 68

Isologous isolated islets of Langerhans were transplanted into the peritoneum and through the portal vein into the liver of diabetic rats. This resulted in the normalization of fasting blood glucose levels, with clear improvement of glucose tolerance tests. The results after intrahepatic implantation were better than after intraperitoneal implantation. Three months after implantation of islets into the peritoneum diabetes recurred and after one year only 2 of the 15 rats were alive, with high blood glucoe levels. In the group with intrahepatic islets the normalization of blood glucose was maintained over a period of one year. Immunohistochemical insulin proofs were positive in the peritoneum over a period of 3 months and in the liver up to one year after implantation. Glucagon proofs were positive in the intraperitoneal islets for 6 weeks and in intrahepatic ones for one year. Morphological examination of transplanted islets suggested that the liver is better suited for islet transplantation than the peritoneum.
Acta Diabetol Lat
PMID:Transplantation of isologous islets of Langerhans in diabetic rats. Long-term immunohistochemical results. 41 14

The metabolic and hormonal changes during a standard physical exercise were studied in healthy subjects and in insulin-dependent diabetics well matched for body weight, and therefore submitted to a similar work load in a physiologic range, and in obese subjects that, owing to their weight, faced a significant heavier work in the same environmental conditions. Moderate work load did not lead to significant changes in metabolic and hormonal blood parameters (blood glucose, FFA and glycerol; insulin, glucagon, growth hormone and cortisol) in healthy subjects. A similar substrate homeostatis was seen in insulin-dependent diabetics, that however showed marked hormonal alterations. In these subjects, indeed, higher levels of plasma glucagon and GH were reached during work and in the recovery phase. Obese subjects, submitted to a heavier work load, presented a marked increase in blood glucose and glycerol which agrees with high GH and cortisol levels, and a subsequent increment of IRI which corresponds to a normalization of blood glucose and glycerol. Obese subjects, therefore, show a normal sensitivity to work load. Considerations about the work load in everyday life are discussed.
Acta Diabetol Lat
PMID:Metabolic and hormonal changes during exercise in healthy, diabetic and obese subjects. 45 17

In order to study endocrine and metabolic responses to normal food ingestion, 8 'healthy' subjects received a standard mixed meal which reflected the composition of Western diet (CHO 47%, protein 23%, fat 26%, alcohol 4%), in 20 min. Before and after the meal, in each subject glucose, lactate, FFA, insulin, C-peptide, glucagon and HGH were determined. The results showed that glycemic and insulinemic responses were not very different from those observed after the classical oral glucose tolerance test. Plasma FFA and blood lactate decreased progressively after the meal. Plasma glucagon and HGH showed opposite changes: pancreatic glucagon rose and HGH slightly declined after composite food ingestion.
Acta Diabetol Lat
PMID:Metabolic and endocrine responses to a standard mixed meal. A physiologic study. 45 19

The aim of this study was to compare the metabolic and hormonal effects of somatostatin to those of propranolol, a beta-adrenergic blocking agent known to reduce basal insulin secretion. For this purpose, 6 normal subjects received somatostatin (4 microgram/min) per 60 min and 6 subjects were infused with propranolol (0.08 mg/min). Somatostatin resulted in a significant decrease of basal insulin (p less than 0.05) and glucagon (p less than 0.01) and raised plasma FFA levels from a mean basal value of 417 +/- 24 muEq/1 (x +/- SEM) to 600 +/- 46 muEq/1 at 60 min (p less than 0.01). Propranolol significantly decreased basal insulin (p less than 0.05) and glucagon (p less than 0.05); FFA levels rose slightly at the end of propranolol administration (p less than 0.05). The levels of FFA which were significantly higher (p less than 0.025) during somatostatin as compared to those observed during propranolol, seem to suggest a role for this tetradecapeptide in lipid metabolism independent of its inhibiting action on islet hormone release.
Acta Diabetol Lat
PMID:A comparative study of metabolic and hormonal responses to somatostatin and propranolol in man. 45 22

Tolbutamide (25 mg/kg: maximum 1 mg) intravenously (IV) and glucagon (0.03 mg/kg; maximum 1 mg) intramuscularly (IM) were given sequentially to 12 untreated girls with XO-Turner's syndrome (ages 6.5 to 17.0 years) and to ten female siblings (ages 8.0 to 16.7 years) to evaluate blood sugar (BS), plasma free fatty acids (FFA), serum immunoreactive insulin (IRI), and growth hormone (IRGH) responses to these insulinogenic secretagogues in order to appreciate any differences of genotypes on carbohydrate metabolism within identical family backgrounds. Seven of 12 patients with Turner's syndrome (58%) but none of the siblings were 20% or more overweight for height. There was a family history of diabetes mellitus in 7 to 12 patients (58%). The results showed significant elevations of mean FFA levels and decreased mean IRI responses to both insulinogenic stimuli without differences in mean BS or serum IRGH responses in the Turner's syndrome patients when compared to the controls. Three of 12 patients (25%) had abnormally elevated and prolonged blood sugar responses to IM glucagon. These findings show a significant incidence of abnormal carbohydrate and lipid metabolism and insulin deficiency in untreated patients with XO-Turner's syndrome when compared to normal female siblings and implicate this chromosomal defect in the impaired insulin secretion.
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PMID:Turner's syndrome and carbohydrate metabolism. I. Impaired insulin secretion after tolbutamide and glucagon stimulation tests: evidence of insulin deficiency. 46 42

Ten children with XO gonadal dysgenesis and ten control siblings (CS) had sequential IV tolbutamide and IM glucagon tests to ascertain serum and salivary insulin concentrations, to confirm the presence of parotid salivary insulin and to determine if these concentrations were of diagnostic value in the diagnosis of insulin deficiency. After tolbutamide, peak serum insulin concentrations were lower in the patients with Turner's syndrome (TS) than in control siblings (58 +/- 10 vs 90 +/- 15 microU/ml) and fractional areas under insulin curves were significantly lower in the patients with Turner's syndrome at 10 to 15 minutes (TS: 240 +/- 16 microUmin/ml; CS: 340 +/- 46 microU-min/ml, P less than 0.05) and at 15 to 30 minutes (TS: 562 +/- 62 microU-min/ml; CS: 884 +/- 128 microU-min/ml, P less than 0.05). After glucagon, peak serum insulin concentrations were significantly lower in Turner's syndrome than in control siblings(P less than 0.02, at 45 minutes) and fractional areas under insulin curves were also lower in TS than in siblings at 30 to 45 minutes (TS: 1,062 +/- 185 microU-min/ml; CS: 2,189 +/- 402 microU-min/ml, P less than 0.02). Basal salivary immunoreactive insulin (IR) concentrations were similar in both groups: TS: 4.8 +/- 2.1 microU/min; CS: 2.1 +/- 0.4 microU/min. Peak salivary IRI concentrations after tolbutamide were 13.8 +/- 4.7 microU/min in Turner's syndrome and 8.8 +/- 1.8 microU/ml in control siblings. Peak salivary IRI values in Turner's syndrome and in control siblings after glucagon were 26.8 +/- 10.1 and 13.4 +/- 2.1 microU/min, respectively. While significant differces in insulin secretion in serum were detected in the two patient groups, no differences were noted between groups when salivary insulin concentrations were compared. These data confirm serum insulin deficiency in gonadal dysgenesis, the presence of immunoreactive insulin in parotid saliva, and suggest the possibility that extrapancreatic insulin synthesis could occur in the parotid gland.
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PMID:Turner's syndrome and carbohydrate metabolism. II. Parotid salivary insulin concentration in normal subjects and in patients with gonadal dysgenesis. 46 43

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.
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PMID:Serum C-peptide in renal failure patients following stimulation of pancreatic secretion. 47 46

The effects of acetylsalicylic acid (ASA), a known inhibitor of prostaglandin (PG) synthesis, on plasma glucose, insulin, glucagon and growth hormone (GH) responses to tolbutamide were examined in ten normal volunteers. Treatment with 3.2 g ASA daily for 3 days caused a significant reduction in basal plasma glucose levels (p less than 0.05); by contrast, basal insulin rose from 23 +/- 2 to 31 +/- 2 microU/ml (p less than 0.01). No significant changes in the basal concentrations of glucagon and GH were found after ASA. Insulin response to tolbutamide was significantly augmented after ASA (p less than 0.01) while GH response to hypoglycemia was reduced (p less than 0.05). The pattern of plasma glucose and glucagon was not significantly modified by the treatment. Since ASA seems to have an action opposite to PGE on insulin and GH secretion, it is possible that the ASA may work through inhibition of PG synthesis.
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PMID:Influence of acetylsalicylic acid on plasma glucose, insulin, glucagon, and growth hormone levels following tolbutamide stimulation in man. 48 Dec 13


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