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)

Effects of a 24 hour fast were studied in 21 obese children aged 7 to 14 and in 8 controls. Mean blood glucose (BG) during fast dropped more in controls (0.88 to 0.54 g/l) than in obese (0.90 to 0.63 g/l) Plasma cortisol changes were similar in the 2 groups, FFA increased (p less than 0.01) in the 2 groups, but the 24 hour mean level was higher in controls (4.0 mEq/l) than in obese (2.06 mEq/l). At the end of the fast, a ketonuria was present in all obese children except 2. Serum alanine dropped similarly in obese (28 to 24 muM p. cent ml) and in controls (30 to 22 muM p. cent ml). All obese exhibited at the end of the fast a significant rise (p less than 0.01) of branched chain aminoacids, not observed in controls. Responses to glucagon (0.03 mg/kg I.M.) were studied before and after fast. At time 0, BG response was higher and more prolonged in obese in spite of hyperinsulinism. At time 24 hours, BG raised from 0.50 to 0.74 g/1 and insulin from 8 to 35 muU/ml in controls, while in obese BG raised from 0.63 to 1.06 g/l and insulin from 25 to 88 muU/ml. Concomitant hyperinsulinsim and biological criteria of hypoinsulinism demonstrated in obese children the peripheral resistance to insulin. The contrast between a normal degree of protein gluconeogenesis and a reduced rate of fat mobilization during fast may be a major biological feature of obesity in childhood.
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PMID:Effect of 24 hour fast in obese children. 100 33

The hepatic and portal productions of acetoacetate and beta-hydroxybutyrate and lipolysis were studied in normal and insulin-controlled alloxan-diabetic sheep. Since hyperinsulinemia is associated with glucagon administration, the latter group of sheep were used to maintain constant plasma insulin levels. After control values were obtained glucagon was infused intraportally at 90 mug/hr for two hours. The ketone body production by portal drained viscera was not significantly affected by glucagon. In alloxanized sheep, glucagon significantly (P less than 0.01) increased net hepatic production of acetoacetate (from -0.54 +/- 0.08 to 0.46 +/- 0.07 g/hr). Lipolysis also increased. However, in the normal sheep, hyperinsulinemia prevented any stimulatory effect of glucagon on hepatic ketogenesis and lipolysis. Therefore, while glucagon appears capable of stimulating ketogenesis andlipolysis, these effects are readily suppressed by insulin.
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PMID:Effects of glucagon and insulin on lipolysis and ketogenesis in sheep. 100 Mar 86

The hormone-substrate milieu has been investigated in male fasted lean (C57BL/6-+/+) mice and mutant obese mice of the same strain (C57BL/6-obob). The lean mouse, in winter, mobilized insufficient fat (due to inadequate stores) to permit survival beyong 3 days and was unable to achieve any degree of conservation of vital protein stores. By contrast, in summer, the same animals survived 7 days and showed evidence of greater and more sustained fat mobilization and ketosis and the ability to conserve protein. The insulin, glucagon, and insulin/glucagon molar ratios changed in both groups in a direction consistent with conversion to a catabolic state, and hence were probably largely responsible for the mobilization of substrates and stimulation of gluconeogenesis and ketogenesis. The seasonal difference in response is unexplained. The obob mice, generally employed as a model for obesity, hyperglycemia, and hyperinsulinemia showed these features but also adapted to fasting in a fashion permitting prolonged survival during this state. In a fashion analogous to that known to occur in man, these animals developed fall in glycemia, rise in circulating fat-derived substrates, and marked protein conservation. Profound fall in insulinemia was associated with a fall in glucagonemia, the latter from normal levels. Thus the initial markedly "anabolic" insulin/glucagon molar ratio diminished, but nevertheless remained higher than at any time in the lean mice. Pancreatic contents of insulin showed markedly different changes with fasting in obob compared with lean mice. The ability of the obese mouse to adapt to prolonged fasting in a fashion largely analogous to that of man renders it a useful model for the study of metabolism in this state, with the potential of applicability of findings to man.
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PMID:Hormone-substrate responses to total fasting in lean and obese mice. 109 42

Factitious hyperinsulinism was suspected in a patient with an 11-year history of insulin-dependent, ketosis-prone diabetes mellitus who began to experience repetitive episodes of "spontaneous" hypoglycemia. Insulin mediation of the hypoglycemia was confirmed by documenting that urinary insulin and total extractable insulin in plasma increased during periods of hypoglycemia. Failure to detect significant amounts of human C-peptide by radioimmunoassay during periods of hypoglycemia or in response to stimulation with glucagon, leucine, or tolbutamide indicated that the insulin was not endogenous. The diagnosis of factitious hyperinsulinism was ultimately proved by the finding of radioactivity in the patient's urine after 131-I Hippuran was added to a vial of insulin found in the patient's room.
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PMID:Plasma C-peptide and diagnosis of factitious hyperinsulinism. Study of an insulin-dependent diabetic patient with "spontaneous" hypoglycemia. 111 42

A patient with a posterior mediastinal malignant neurofibrosarcoma and recurrent episodes of severe hypoglycemia was demonstrated to have basal hyperinsulinemia on repeated study. Despite hypoglycemia, there was no glucagon response to aminogenic stimulation. No immunoreactive insulin was detected on extraction of the tumor and no secretory granules of beta type were seen on electron microscopic examination of tumor tissue. Following tumor removal, plasma glucose and insulin levels returned to normal. Alpha cell function improved. These findings suggest stimulation of pancreatic beta cell secretion and possible inhibition of alpha cell response by an extrapancreatic tumor.
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PMID:Hyperinsulinemic hypoglycemia associated with a neurofibrosarcoma. 113 Sep 33

Net hepatic uptakes of plasma alanine (Ala), glutamate (Glu), and glutamine (Gln) were measured before and during intraportal glucagon infusions in five normaland four insulin-and alloxan-treated (ITA), conscious, fed sheep. Since hyperinsulinemia is associated with glucagon administration, ITA sheep were used so that constant plasma insulin levels could be maintained. Glucose turnover was determined by a vena caval infusion of glucose-6-'3H. In addition, in ITA sheep, Ala-'14C wasinfused for measurement of plasma Ala turnover, its unidirectional organ metabolism, and contribution to glucose synthesis. During infusion of glucagon, the net hepatic uptake of Ala increased significantly (P is less than 0.01) from control values of 3.8 plus or minus 0.5 and 2.7 plus or minus 0.6 mmol/h to 5.9 plus or minus 1.0 and 5.5 plus or minus 0.8 mmol/h in normal and ITA sheep, respectively. Similarly, Gin uptake increased from 4.3 plus or minus 1.4 and 1.6 plus or minus 0.5 to 5.5 plus or minus1.6 and 3.7 plus or minus 1.0 mmol/h, respectively. The conversion of Ala to glucose increased from control values of 1.7 plus or minus 0.5 to 3.0 plus or minus 0.5 mmol/h. Arterial plasma Ala and Gin concentrations decreased about 25% during glucagon administration, presumably as a result of their increased hepatic uptakes. A decreasein utilization of plasma Ala, but no change in production was calculated for the nonhepatic tissues, indicating that glucagon increased gluconeogenesis from Ala at the expense of muscle protein synthesis. Glucagon thus has a direct effect on the liver butonly an indirect effect on other tissues.
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PMID:Effect of glucagon on plasma alanine and glutamine metabolism and hepatic gluconeogenesis in sheep. 115 95

The net hepatic metabolism of amino glycerol, lactate, and pyruvate was determined in conscious fed sheep by multiplying the venoarterial concentration differences by the hepatic blood or plasma flow. In each experiment several sets of control blood samples were taken; glucagon or insulin then was infused intraportally for 2 h during which additional samples were taken. Four types of experiments were performed: 1) glucagon infusion (150 mug/h) into normal sheep, 2) glucagon infusion (100 mug/h) into insulin-treated alloxanized sheep, 3) insulin infusion (1.17 U/h) into normal sheep, and 4) insulin plus glucose infusion (12.3 mmol/h) into normal sheep. The second group of experiments was performed to prevent reflex hyperinsulinemia, and the fourth was performed to prevent reflex hyperglucagonemia. Glucagon directly stimulated the net hepatic uptake of alanine, glycine, glutamine, arginine, asparagine, threonine, serine, and lactate. Glucagon also stimulated lipolysis in adipose tissue. Insulin, on the other hand, appeared to have a lipogenic effect on adipose tissue and to stimulate directly the uptake of valine, isoleucine, leucine, tyrosine, lysine, and alanine only at extrahepatic sites. The study showed that, in sheep, the effects of glucagon primarily are on liver, and insulin's effects primarily are on skeletal muscle and adipose tissue where it promotes protein and lipid synthesis.
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PMID:Effects of glucagon and insulin on net hepatic metabolism of glucose precursors in sheep. 120 Jan 53

Increased plasma pancreatic glucagon concentrations have been reported during various states of decreased glucose tolerance. In vitro studies have demonstrated that human somatomammotropin stimulates glucagon release. The present investigation aimed at evaluating the role of plasma flucagon in the insulin resistance associated with normal pregnancy. Postprandial samples of plasma were obtained from 156 pregnant women between the 5th and the 40th week of pregnancy and were assayed for blood glucose, plasma insulin, glucagon and free fatty acids. Plasma insulin showed a gradual increase during pregnancy, and reached its maximal values during the last trimester. A moderate but significant increase in plasma glucagon was present between the 16th and the 28th week of gestation, whereas during the first and the last trimester of pregnancy its concentration was similar to that in non pregnant women. Intravenous glucose tolerance was performed during the last trimester and in a group of non pregnant control women. The slight decrease in glucose tolerance and the marked hyperinsulinemia associated with late pregnancy were accompanied by a more rapid and more pronounced decrease in plasma glucagon. A rapid and sustained decrease in glucagon was also observed when plasma FFA were raised by the intravenous administration of a triglyceride emulsion and heparin. These data suggest that glucagon is not involved in the insulin resistance associated with normal human pregnancy.
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PMID:Plasma glucagon levels in normal women during pregnancy. 120 23

Neurotensin and substance P given iv 5, 10, 20 and 30 minutes prior to blood collection produce hypoinsulinemia, hyperglucagonemia and hyperglycemia in the rat. Glucagon similarly produces hyperglycemia in rats but results in hyperinsulinemia. On a molar basis neurotensin is ca. 10 and 30 times more active in inducing hyperglycemia than substance P and glucagon, respectively. The enhanced glucogenic effects of neurotensin and substance P over glucagon may well result from their inhibition of insulin release. Neurotensin and substance P may be important in glucose homeostasis.
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PMID:Effects of neurotensin and substance P on plasma insulin, glucagon and glucose levels. 126 3

Among 33 patients with endocrine pancreatic tumors due to multiple endocrine neoplasia type 1 (MEN-1), 19 (58%) patients had hypergastrinemia, 7 (21%) patients had hyperinsulinism, and 7 (21%) patients had clinically non-functioning lesions. At least one gross tumor was found in all patients undergoing pancreatic surgery, including those with negative localization studies prior to operation. The patients also had additional macroscopic tumors as well as numerous microadenomas, and the lesions frequently were positive for immunostaining with multiple hormones, mainly pancreatic polypeptide, insulin, glucagon, and somatostatin. Duodenal endocrine lesions were found in 4 of 5 investigated patients and stained with gastrin and somatostatin antibodies. Distal, mainly subtotal pancreatic resection, was performed in 18 patients, eventually combined with caput tumor enucleation or duodenotomy, while a few patients underwent only tumor enucleation or a Whipple procedure. The long-term outcome of operation was most favorable in patients with hyperinsulinism; only 1 patient had clinical recurrence. Patients with hypergastrinemia experienced only transitory lowering of serum gastrin values after pancreatic surgery and 47% of them had or developed metastases. Such tumor spread was seen in 57% of the patients with non-functioning lesions. Nine patients died from progressive tumor disease during follow-up. Consistent with previous studies, we found that surgery is indicated in MEN-1 patients with hyperinsulinism even if a lesion is not visualized by radiology. In addition, these indications should be extended to also include patients with only biochemical markers of disease, including elevations of gastrin, as these indicate the presence of gross tumors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pancreatic tumors in multiple endocrine neoplasia type 1: clinical presentation and surgical treatment. 135 27


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