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)

To investigate the effects of insulin and sulfonylurea drug administration on islet A and B-cell functions, insulin and glucagon response was studied in normal rats treated with insulin (4 U/day subcutaneously) or glibenclamide (0.03 mg/kg intraperitoneally) for 8 weeks. In intravenous glucose tolerance test (0.5 g/kg), lower insulin response and impaired glucose tolerance were observed in insulin-treated rats and higher insulin response and impaired glucose tolerance were observed in glibenclamide-treated rats. In perfused pancreas, insulin response to glucose and arginine was significantly lower in insulin-treated rats and that was significantly higher in glibenclamide-treated rats. Glucagon response was not altered by insulin or glibenclamide treatment. These results suggest that hyperinsulinisation and glibenclamide administration strongly influence pancreatic B-cell function but not influence pancreatic A-cell function.
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PMID:Effect of long-term administration of insulin and glibenclamide on pancreatic A and B cell function. 211 4

Injections of glucagon in dairy cows resulted in a rapid and marked increase in serum insulin and also in plasma glucose. Glucagon injection appears to be a simple and useful method for testing insulin secretion and glucose release. There was a somewhat reduced insulin response 2 weeks after calving in normal cows. Cows given high intensity feeding before calving showed higher plasma glucose levels in the glucagon test 3 days post partum and showed signs of reduced sensitivity to insulin action. Cows with abomasal displacement showed impaired glucose tolerance and heterogeneity of insulin responses indicating insulin resistance and signs of Type 2 (non-insulin-dependent) diabetes mellitus.
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PMID:Impaired glucose tolerance and heterogeneity of insulin responses in cows with abomasal displacement. 212 Aug 68

The authors carried out a self-controlled study using 11, non-obese patients with impaired glucose tolerance. The first day an oral glucose tolerance test was performed as a control. This was repeated the next day with a simultaneous intake of 20 g natural wheat bran. On both days blood samples were taken at 30 minute intervals (for three hours period) after glucose or glucose plus bran ingestion to measure the plasma sugar, insulin, C-peptid, gastrin and glucagon levels. It has been found that: 1. With simultaneous bran intake the blood glucose levels were decreased as compared to the control values. 2. The serum insulin, and C-peptid levels were similar in both tests. 3. The glucagon response curve fell below that of the control. 4. The serum gastrin levels did not show any change following either glucose or glucose plus bran intake. It has been concluded, that the dietary fibres are able to decrease of glucagon release, beside their direct inhibitory effect on the level of sugar absorption from gastrointestinal tract.
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PMID:[Hormonal changes during administration of dietary fibers in patients with decreased glucose tolerance]. 215 75

Cyclosporine has been shown to cause glucose intolerance in both humans and animals. This can result from alterations in insulin release, insulin metabolism, the sensitivity of peripheral or hepatic tissues to insulin, or a combination of these factors. The present study was designed to simultaneously evaluate the effect of CsA on these variables. A group of chronically catheterized dogs were administered oral CsA (20 mg/kg/day) for a period of 10 weeks. The glucagon stimulation test (GST) and the euglycemic glucose clamp technique, using a primed continuous infusion of 3H-3-glucose and a continuous insulin infusion (0.8 mU/kg/min), were employed to evaluate pancreatic insulin release, peripheral glucose disposal rate (Rd), hepatic glucose output (HGO), and metabolic clearance rate (MCR) of insulin. The dogs were tested before and after 2, 6, and 10 weeks of CsA administration. Serum CsA levels were 358 +/- 85, 244 +/- 48, and 355 +/- 81 ng/ml at 2, 6, and 10 weeks, respectively (P = NS). Elevated fasting glucose and an abnormal glucose response to an i.v. bolus of glucagon (0.25 U) were noted after 2, 6, and 10 weeks of CsA administration. The areas under the glucose curve (AUCG) for 0-60 min were 9605 +/- 773, 11634 +/- 1226, 12380 +/- 719, and 12626 +/- 1560 mg/min/dl at 0, 2, 6, and 10 weeks, P(F3, 15 = 5.1) = 0.012, demonstrating a CsA-induced disturbance of glucose homeostasis. The areas under the insulin curve (AUCI) for 0-20 min of the insulin response curve were 2033 +/- 203, 1089 +/- 187, 1038 +/- 179, and 972 +/- 161 uU/min/dl at 0, 2, 6, and 10 weeks, P(F3, 15 = 13.1) less than 0.001, indicating a 50% reduction during CsA treatment. CsA did not affect basal Rd, but peripheral insulin resistance was noted in the insulin-stimulated state. Rd during the third hour of the insulin infusion decreased from 6.72 +/- 0.69 to 4.42 +/- 0.44, 5.02 +/- 0.64, 4.47 +/- 0.52 mg/kg/min at 0, 2, 6, and 10 weeks, respectively, P(F3, 15 = 6.94) less than 0.004. HGO suppression by insulin and MCR of insulin were not altered by CsA. Similarly, glucagon secretion did not appear to be influenced by CsA. In conclusion, this study has simultaneously evaluated the effect of CsA on several aspects of glucose and insulin metabolism in the dog. CsA administration produces abnormal glucose homeostasis by reducing pancreatic insulin release, in addition to inducing peripheral insulin resistance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Inhibition of insulin release by cyclosporine and production of peripheral insulin resistance in the dog. 218 Jan 52

Intermittent hepatic dearterialization is used in the palliative treatment of liver malignancy. However, its metabolic consequences are not established. Therefore the influences of the procedure on the plasma insulin, glucagon and glucose responses were studied in healthy rats and in rats with a tumour inoculated subcapsularly into the liver. To study the influence on stimulated islet hormone secretion we infused arginine intravenously (7 mg/min) for 30 min, because arginine is known to stimulate the secretion of both insulin and glucagon. During hepatic dearterialization, hyperglycaemia developed; mean(s.e.m.) blood glucose levels after 60 min of dearterialization were 20.2(1.3) mM versus 14.7(1.5)mM in controls (P less than 0.001). Concomitantly, compensatory hyperinsulinaemia and hypoglucagonaemia occurred. Furthermore, during both dearterialization and in the immediate reperfusion phase, the arginine-induced increase in plasma insulin levels was impaired (P less than 0.001), whereas the arginine-induced increase in plasma glucagon levels was not significantly affected. These changes were qualitatively the same in tumour-free and tumour-bearing rats. We conclude that glucose intolerance develops during selective hepatic dearterialization, which is evident both from basal hyperglycaemia and impaired insulin secretion.
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PMID:Intermittent hepatic dearterialization induces glucose intolerance: an experimental study in the rat. 218 62

Although estradiol (E2) is considered primarily for its role in reproduction, it can exert numerous physiological actions on a variety of tissues. However, there are several difficulties in isolating these actions and determining its impact for in vivo situations. Despite the limitations, it does appear that E2 can alter, under certain conditions, resting and acute exercise metabolism and blood glucose regulation. Specifically, E2 can increase lipid availability and utilization and decrease gluconeogenesis and glycogenolysis. Development of glucose intolerance as a result of insulin insensitivity has also been documented. The mechanisms of E2 may be through direct alterations in key enzyme activity and membrane permeability or indirectly via changes in insulin:glucagon, cortisol, hGH, and catecholamine levels or sensitivity. Future research should focus on understanding the effects of exercise and diet on chronic E2 status and the resulting impact for a variety of conditions that include reproductive and skeletal integrity and predisposing metabolic risk factors for CAD and diabetes. In order to make meaningful correlations between E2 levels and physiological measurements such as bone mineral content, lipid profiles, glucose intolerance, etc., there needs to be a standard guideline for determining and defining one's "estrogen status." Finally, in order to identify underlying mechanisms, an understanding of and appreciation for the interrelationships among the numerous compositional, metabolic, and (neuro)endocrine factors involved is needed. A general model is presented, along with specific applications, to study these interactions.
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PMID:Metabolic actions of estradiol: significance for acute and chronic exercise responses. 219 50

This study investigated insulin sensitivity and glucose tolerance after subtotal pancreatectomy for carcinoma of the head of the pancreas. Twelve consecutive, non-diabetic patients were studied after potentially curative surgery at which the distal pancreas was stapled off, leaving approximately 15% of the pancreas in situ. Brief infusions of insulin (10 mU kg-1) and glucose (25 g) were given before and 4 days after operation. Postoperatively, blood glucose levels remained unchanged, whereas fasting levels of insulin. C-peptide, and pancreatic glucagon were decreased, although significantly (p less than 0.01) only for glucagon. The early and late phases of the insulin and C-peptide responses to glucose were severely reduced. Notably, the hypoglycemic action of insulin and the glucose tolerance were similar to those observed before operation. It is concluded that an acute reduction in pancreatic mass does not impair insulin action or glucose tolerance shortly after surgery. This contrasts with the insulin resistance and glucose intolerance seen shortly after pancreas-preserving intra-abdominal procedures of similar size. It is suggested that the decrease in glucagon levels is at least partly responsible for the preservation of insulin action after subtotal pancreatectomy.
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PMID:Reduced insulin secretion by subtotal pancreatectomy: preservation of insulin sensitivity and glucose tolerance in postoperative patients. 220 4

To evaluate the contribution of the splanchnic area to the carbohydrate abnormalities associated with chronic uremia, the splanchnic exchange of glucose and gluconeogenic substrates was quantitated basally and after an iv glucose load in nine uremic patients with impaired glucose tolerance and seven control subjects. In the basal state, blood glucose and splanchnic glucose production were similar in the two groups. During glucose infusion (33 mumol/kg.min for 90 min), blood glucose reached significantly higher levels in the uremic patients than in controls (P less than 0.02). Plasma insulin increased slightly more in uremic patients than in controls (P less than 0.05 at 15 min). Both basal and postglucose glucagon levels were 2- to 3-fold higher in uremic patients than in normal subjects (P less than 0.05-0.02). In both groups, splanchnic glucose balance switched from net output in the basal state (-9.4 +/- 0.5 and -8.0 +/- 1.1 mumol/kg.min in normals and uremics, respectively) to net uptake with glucose infusion. However, this response was less marked in the uremic patients than in normal subjects (P less than 0.05-0.02 at 30 and 90 min). The cumulative net splanchnic glucose balance over the 90-min study period was 538 +/- 55 mumol/kg in normal subjects and 279 +/- 89 in uremic subjects (P less than 0.05). A net splanchnic lactate uptake was present in the basal state in normal (4.2 +/- 0.5 mumol/kg.min) and uremic subjects (3.4 +/- 0.5). During glucose infusion, in normal subjects splanchnic lactate exchange switched to a net output (-4.0 +/- 1.6 mumol/kg.min), whereas in the uremic group it remained as a net uptake (1.1 +/- 0.7) throughout the study period. Splanchnic gluconeogenic amino acid uptake was similar in the two groups in the basal state (1.8 +/- 0.1 mumol/kg.min and 2.2 +/- 0.2 in normal and uremic subjects, respectively). Glucose infusion caused a marked fall in amino acid uptake by liver in normal subjects, whereas no change was observed in the uremic group (0.9 +/- 0.3 and 1.9 +/- 0.2 mumol/kg.min, respectively). Splanchnic glycerol uptake was not different in the two groups in the basal state (0.75 +/- 0.2 and 1.1 +/- 0.2 mumol/kg.min) and decreased to a similar extent during glucose infusion. We conclude the following. 1) In uremic patients with glucose intolerance but normal fasting glycemia, the splanchnic metabolism of glucose and gluconeogenic substrates is normal in the postabsorptive state.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of the splanchnic tissues in the pathogenesis of altered carbohydrate metabolism in patients with chronic renal failure. 240 70

The endocrine pancreatic functions were evaluated in 19 patients with pancreatic head cancer by measuring plasma immunoreactive pancreatic glucagon (IRG) and insulin (IRI) responses to an intravenous dose of 30 g of arginine. The IRG responses differed by level of urinary amylase excretion, degree of glucose intolerance and degree of exocrine insufficiency. Higher IRG responses were observed in the nondiabetic subset, the hyperamylasuric subset, and the mild to moderate exocrine insufficient subset than in the corresponding opposites. Even higher responses were also found in the subset with all 3 characteristics, suggesting better preservation of the pancreatic tissue, than in that with 2 or fewer. The results obtained suggest that A-cell function increases in the earlier stages of pancreatic head cancer.
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PMID:Pancreatic A- and B-cell responses to intravenous arginine in cancer of the head of the pancreas: relation to clinical features. 241 2

Intracellular Ca2+ influx is an essential step in insulin (I) release. Calcium antagonists are reported to reduce I release in vitro and in patients with impaired glucose tolerance (IGT) during acute administration. Their effects during long-term therapy are still controversial. To evaluate the effects of chronic verapamil (V) and nifedipine (N) on carbohydrate metabolism, 12 hypertensive patients (WHO II; aged 37-64 years) with IGT underwent intravenous glucose tolerance tests (IVGTT) (0.33 g/kg body weight in 3 min), arginine (A) infusion (30 g/30 min), and hypoglycemic stress (regular insulin 0.15 U/kg body weight) during which blood levels of glucose (G), I, growth hormone (GH), glucagon (IRG), and cortisol (C) were measured. The patients were then randomized to V (120 mg b.i.d.) or N (20 mg b.i.d.) treatment and, 1 month later, both IVGTT and A infusion were repeated. Hormone determinations were performed by the radioimmunoassay (RIA) and G by the enzymatic method. The patients were maintained on their usual diet for the duration of the study. The rate of decline of G during IVGTT was expressed as Conard's K coefficient (K; normal values greater than 1.3). I and GH during IVGTT were evaluated as the differences between basal and peak values. I, IRG, and GH during A infusion were analyzed as incremental areas. Our results show that neither V nor N impaired carbohydrate metabolism in hypertensive patients with IGT.
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PMID:Effect of nifedipine and verapamil on carbohydrate metabolism in hypertensive patients with impaired glucose tolerance. 245 32


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