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)

Insulin and glucagon have been studied in 20 subjects (both of the subjects' parents were diabetic or in case of only one diabetic parent, the other showed a first degree familiarity of diabetes): 10 showed normal glucose tolerance ('true prediabetics') and 10 impaired glucose tolerance ('genetic chemical diabetes'). Mean insulin response to oral (100 g) and i.v. glucose load (200 mg/kg followed by 20 mg/kg/min for 60 min) and to arginine infusion (25 g in 30 min) was normal in the prediabetics and delayed and higher in the subjects with chemical diabetes as compared to the control group. Glucagon response to arginine was higher, but not significantly, in prediabetics and in subjects with chemical diabetes. In both of these groups glucagon suppression by glucose was not observed. The insulin/glucagon molar ratio was significantly reduced after glucose infusion in these two groups. No correlation was found between insulin and glucagon secretion after arginine or glucose. A possible alteration in the mechanism controlling glucagon secretion even in the earliest phases of diabetes is suggested.
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PMID:Glucagon and insulin secretion in potential diabetes. 36 Jul 48

Arginine infusion tests were carried out in seven patients with pheochromocytoma before and after extirpation of the tumors in order to evaluate pancreatic islet alpha- and beta-cell function during the state of endogenous catecholamine excess. Six of the patients had glucose intolerance; one did not. Preoperatively, the pancreatic glucagon response was suppressed, while the insulin response was comparable to that in normal control subjects. Plasma glucose levels decreased rapidly after the beginning of arginine infusion in all patients. Theses changes during the infusion were evident in the one patient without glucose intolerance. Postoperatively, the glucagon response and plasma glucose changes were normalized. In addition to the obvious suppression of pancreatic alpha-cell function in our patients with pheochromocytoma, it seems likely that pancreatic beta-cell function also was suppressed; there was no enhancement of the insulin response to arginine during the period of chronic hyperglycemia, a situation in which a synergistic effect between glucose and arginine might be expected.
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PMID:Pancreatic alpha- and beta-cell function in pheochromocytoma. 38 21

Intravenous hyperalimentation allows complete nutrition and anabolism in patients who cannot be fed by the oral route. However, several complications have been reported, e.g. septicaemia and hyperglycaemina. In 51 intensive-care patients receiving hyperalimentation, 18% were found to be hyperglycaemic in spite of insulin administration. Hyperglycaemia was frequently associated with stress. In 8 patients undergoing major surgery, which was chosen as a stress model, decreased insulin and increased glucagon, growth hormone and cortisone levels were observed. These findings could explain stress-induced glucose intolerance. In a further experiment, 8 intensive-care patients were given alternative intravenous feedings with either 600g of a mixture of glucose, fructose and xylitol in a ration of 1:2:1 or 600g glucose per day. During both regimens insulin administration was required in 4 patients, but the insulin dosage was lower with the mixture. Plasma glucose during glucose infusion was 205+/-25mg/100ml(M+/-SEM) and the sum of plasma glucose, fructose and xylitol during infusion of the mixture was 176+/-33mg/100ml, the difference being of borderline significance (p less than 0.05). The advantages and disadvantages of infusable substrates are summarized on the basis of the available literature and it is concluded that, in general, glucose is preferable. However, if hyperglycaemia is difficult to control, partial replacement of glucose by glucose substitutes or fat emulsions may be advantageous. A routine infusion programme for central venous feeding is suggested. Causes and prevention of side-effects are reviewed. In many patients receiving central venous nutrition less hazardous and less expensive methods could be used such as nasogastric tube feeding, elemental diet or peripheral venous nutrition.
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PMID:[Parenteral hyperalimentation (author's transl)]. 40 48

Porphyria cutanea tarda (PCT) has a known increased incidence of diabetes mellitus and hepatic involvement. We investigated glucose tolerance and glucoregulatory hormone alterations in seven patients with PCT and correlated these results with hepatic histology by percutaneous liver biopsy. Abnormal glucose tolerance was observed in six of the seven patients (87%). Fasting serum insulin levels were normal range, and normal glucose and growth hormone responses to standard, exogenous intravenous insulin were observed. Fasting serum glucagon and urine free cortisol levels were normal in those patients in whom they were measured. While varying degrees of abnormalities were found on histopathologic exam of the liver biopsies, no patient met the criteria for cirrhosis, and none of the patients demonstrated abnormal levels of insulin counterregulatory hormones commonly seen in cirrhosis. Thus, liver disease may not be the sole cause of the observed glucose intolerance and hyperinsulinemia in PCT patients.
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PMID:Carbohydrate metabolism in porphyria cutanea tarda. 46 44

Hepatic glucose production and its responses to glucagon and insulin were studied in perfused livers obtained from spiny mice (Acomys cahirinus)--rodents characterized by normoglycemia, decreased glucose tolerance and decreased insulin secretion--and from Swiss albino mice. The dose-response characteristics of glucagon-induced hepatic glucose output were similar in spiny and albino mice. However, maximally stimulated glucose production were significantly lower in the spiny mouse. Furthermore, the liver of the spiny mouse was more sensitive to the action of insulin: 0.5 X 10(-6) M insulin significantly inhibited the action of glucagon in spiny mice but not in albino mice. It is proposed that the increased sensitivity of the hepatic glucose output to insulin and the decreased maximal stimulation by glucagon may be factors that limit the negative effects of the impaired insulin secretion in spiny mice, thereby reducing the severity of the glucose intolerance. Analogous mechanisms may be present in the early stages of the diabetic syndrome in man.
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PMID:Glucose production by the perfused liver of the spiny mouse (Acomys cahirinus): sensitivity to glucagon and insulin. 46 20

Glucose intolerance has been commonly observed in sepsis and has been attributed to a multitude of endocrine and metabolic disorders. From 1977 to 1978, 19 patients were studied using intravenous glucose tolerance tests to evaluate this phenomenon; 15 patients presented with ongoing sepsis and four patients served as stress controls. Glucose intolerance was found to be a significant finding in less than 40% of the septic group. This state of intolerance was noted to be associated with a high mortality rate (60%), whereas glucose tolerance in sepsis was associated with a much improved mortality rate (10%). Hormone levels were correlated with glucose tolerance curves using the parameters of insulin, glucagon, growth hormone, cortisol, and epinephrine levels. Glucose intolerance and a high mortality rate were linked to sustained hyperglucagonemia, which was unresponsive to glucose challenge, and to marked suppression of growth hormone. This apparently represents a decompensated peripheral metabolic energy deficit, which results in the increased mortality rate.
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PMID:The sepsis-glucose intolerance riddle: a hormonal explanation. 47 28

Xylazine is a tranquilizer that is widely used in both biomedical research and veterinary medicine. We now report that in dogs, clinically effective doses of xylazine both markedly decrease basal insulin levels and completely abolish the rise in insulin produced by iv glucose. These changes in insulin levels lead to elevations of fasting plasma glucose and glucose intolerance. In contrast, glucagon levels are unchanged. These studies suggest that xylazine may be a useful agent in the study of glucose metabolism and beta-cell function.
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PMID:Rapid inibition of basal and glucose-stimulated insulin release by xylazine. 47 4

To determine whether glucose intolerance in patients with chronic renal failure could improve by hemodialysis, the effects of arginine infusion on the concentration of blood sugar, insulin, glucagon, growth hormone were examined in healthy volunteers, undialyzed and dialyzed patients with chronic renal failure. Plasma concentrations of sugar and hormones in undialyzed and dialyzed patients responded similarly to arginine infusion. While blood samples were collected at 30, 45, 60, 90, 120 and 180 min after beginning infusion of arginine, the concentrations of sugar and hormones in both patients had no statistically significant differences. However, plasma concentrations of growth hormone in both patients 180 min after beginning of arginine infusion gave statistically significant differences. In the present study, the results suggest that hemodialysis might not improve the glucose tolerance in the patients with chronic renal failure.
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PMID:Response of insulin, glucagon and growth hormone to arginine infusion in patients with chronic renal failure. 49 15

Glucose tolerance and insulin and glucagon secretion were investigated in two groups of uremic patients, respectively on conservative and hemodialytic treatment. For this purpose, a glucose infusion was performed in the fasting state. Glucose intolerance was observed in uremic patients; hemodialysis improved, but did not normalize the glucose disposal. In uremic patients both on conservative and dialytic treatment plasma insulin and glucagon levels were higher than in the control group; the pattern of glucagon suppression was well maintained. The data obtained suggest that glucose intolerance in uremia is related mainly to peripheral insulin resistance and is not due to hyperglucagonemia.
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PMID:Glucose intolerance in uremia (A- and B-cell function during conservative and dialytic management. 61 88

The effect of a 14 day-administration of butylbiguanide was investigated in a group of 10 obese patients with mild-to-moderate glucose intolerance. Glucose tolerance was significantly improved, while fasting blood glucose and plasma levels of free fatty acids, insulin and glucagon remained unchanged. The estimation of the amount of the oral glucose load oxidized into CO2 was performed by means of a recently described procedure using "naturally labelled 13C-glucose" as tracer. The curves depicting the oxidation of the exogenous glucose load were similar in shape and magnitude before and after administration of the biguanide; in the latter case, however, slightly higher rates of oxidation of exogenous glucose were recorded during the 2nd, 3rd and 4th hours of the test. These data do not provide evidence that the biguanide-induced improvement in glucose tolerance in patients with mild-to-moderate glucose intolerance is associated with any inhibiting or delaying effect of this type of drug on intestinal absorption (and subsequent oxidation) of the exogenous glucose load. On the contrary, a slight, but statistically significant, increase in the oxidation of exogenous glucose has been observed after butylbiguanide.
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PMID:Oxidation of an exogenous glucose load using naturally labelled 13C-glucose. Effect of butylbiguanide therapy in obese mildly diabetic subjects. 62 31


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