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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

Serum alanine concentration was determined in nonpregnant and pregnant normal control Swiss albino (SA) and genetically diabetic KK mice. The serum alanine levels were significantly lower in nonpregnant KK than in nonpregnant SA mice. Fasting elicited hypoglycemia, hypoinsulinemia and hypoalaninemia in both groups of pregnant mice. Oral administration of alanine in nonpregnant and pregnant mice resulted in a significant rise in blood sugar levels within 15 min in both groups. However, the initial blood sugar response to oral alanine was greater in pregnant than in nonpregnant mice. This increase in blood sugar response to exogenous alanine appears to be mediated by glucagon. The data suggest that pregnancy elicits hypoglycemia, hypoinsulinemia and hypoalaninemia in both nondiabetic and diabetic mice.
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PMID:Effect of pregnancy on serum alanine concentration in normal and genetically diabetic mice. 100 7

Altogether 17 individual amino acids were determined before and during glucagon infusion in normoglycaemic and hypoglycaemic SGA infants. The magnitude and time course of the response in total plasma amino acids to glucagon infusion (0.2 microng/kg/min for four hours) differed in the two groups: while in the normoglycaemic SGA infants a significant hypoaminoacidaemia was noted by the second hour of glucagon infusion, in the hypoglycaemic newborns no appreciable changes were observed. In the former group altogether twelve amino acids showed a progressive and significant decline. The fall of three important gluconeogenic amino acids alanine, glycine,proline, and that of three branched chain amino acids was particularly striking. In contrast, in the hypoglycaemic infants the amino acids were not significantly affected by glucagon infusion. This unresponsiveness of plasma amino acids was probably transient as judged from the moderate hypoaminoacidaemia noted by the end of the infusion period. The observations seem to have important implications regarding the influence of glucagon on hepatic glucose production, and its possible therapeutic importance in the management of hypoglycaemic intrauterine malnourished infants.
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PMID:The metabolic effects of glucagon infusion in normoglycaemic and hypoglycaemic small-for-gestational-age infants. II. Changes in plasma amino acids. 102 24

To determine if pancreatic glucoregulatory hormones can be implicated in the glucose fall of pregnancy, we have measured plasma immunoreactive insulin and glucagon (IRI and IRG) in rats. Fed rats in midgestation show a rise in IRI without a corresponding increase in IRG. In late gestation, IRG rises significantly, but only enough to keep pace with a further rise in IRI. On a molar basis, IRI remains the predominant hormone despite a marked fall in blood glucose. After a 48-h fast IRI falls to comparably low levels in pregnant and virgin rats. A small rise in IRG is seen in virgin but not in pregnant rats despite frank hypoglycemia in the latter. Thus, IRG secretion in pregnancy is diminished relative to IRI in the fed state and fails to increase in the fasted state despite the stimulus of a lower glucose in both instances. To evaluate IRG secretory reserve, the IRG response to i.v. alanine was assessed in late gestation. In fed rats a greater IRG increase is seen in pregnancy; after fasting no difference is seen between pregnant and virgin rats. These results preclude an absolute deficiency in glucagon secretion. Pancreas hormone stores were alos measured in an effort to explain the altered secretory state. We find reciprocal changes in IRI and IRG content favoring IRG in midgestation and IRI in late gestation. Thus, pancreas hormone storage is altered in pregnancy but does not account for the changes in hormone secretion. Rather, pregnancy exerts an effect on the islet secretory process itself. Release of IRI is enhanced relative to IRG regardless of the blood sugar level. These observations suggest that in the pregnant rat circulating levels of insulin and glucagon may act to limit hepatic glucose output. Available evidence from the literature supports the concept of restrained glucose production. It is proposed that a lower blood glucose production. It is proposed that a lower blood glucose in rat pregnancy may be a lesser liability teleologically than would be the obligate nitrogen wasting which accompanies gluconeogenesis.
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PMID:Plasma glucagon and insulin in rat pregnancy. Roles in glucose homeostasis. 110 77

The effects of oral alanine feeding on glucose homeostasis were evaluated in 21 infants who were small for gestational age and 26 who were appropriate for gestational age. In the first 24 hours, basal plasma alanine concentrations were higher in the former. Oral alanine feedings produced a significant rise over baseline levels of plasma alanine and glucagon concentrations in both groups. The blood glucose and plasma insulin concentrations also increased significantly in infants who were appropriate but not in those who were small for gestational age. At 25 to 96 hours of age, plasma glucagon, insulin and blood glucose concentrations did not change after the alanine feeding in either group. These data indicate that in the normally nourished infant (appropriate forgestational age), gluconeogenic amino acid (alanine) enhances hepatic glucose output. This phenomenon is not observed in the mainourished infants (small for gestational age), a point that may reflect decreased glycogen stores and ineffective gluconeogenic enzyme system in such infants.
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PMID:Effects of oral alanine feeding on blood glucose, plasma glucagon and insulin concentrations in small-for-gestational-age infants. 111 40

Changes in blood levels of glucagon, insulin and glucose in response to infusions of alanine and glycine have been studied in postabsorptive and fasting obese human subjects. Four-to-five-fold elevations of baseline plasma alanine levels stimulated glucagon secretion significantly. Supraphysiological plasma levels of glycine had a small but insignificant stimulatory effect on glucagon secretion. The glucose increase (6 to 10 mg per 100 ml) observed within 30 min of a supraphysiologic alanine infusion in subjects fasted for 2 or more weeks may be secondary to glucagonmediated glycogen breakdown. However, despite equivalent glucagon rises in the other two study periods, no significant rise in blood sugar was noted during the period of infusion.
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PMID:Effect of alanine and glycine on glucagon secretion in postabsorptive and fasting obese man. 111 54

Plasma glucagon levels rose within 1 hr after withdrawal of insulin in 7 juvenile-type diabetics previously kept normoglycemic by prolonged intravenous infusions of insulin. These changes preceded subsequent elevations in plasma alanine levels. Individual rises in plasma glucagon were correlated with elevations in plasma glucose, beta-hydroxybutyrate, free fatty acid, and glycerol levels, suggesting that glucagon may play an important role in the development of diabetic ketoacidosis in man.
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PMID:Plasma glucagon and alanine responses to acute insulin deficiency in man. 111 61

Trypsin and elastase isolated from the pancreas of the moose (Alces alces), a member of the Cervidae (deer) family, were characterized with respect to their amino acid composition and specificity towards polypeptides. Moose trypsin possessed 234 residues, based on alanine recoveries equal to 16.0 residues, with a molecular weight calculated at 24 476. Moose trypsin readily hydrolysed peptide bonds in which the carbonyl group was contributed by arginine, lysine and S-2-aminoethylcysteine as indicated by the peptides isolated following hydrolysis of the oxidized and the S-aminoethylated B-chain of insulin. Moose elastase possessed 231 residues, based on alanine recoveries equal to 17.0 residues, with a molecular weight calculated as 24 201. The high lysine (9 residues), low arginine (3 residues) content was in contrast to the opposite situation with porcine elastase and the elastase-like, alpha-lytic protease from Sorangium. The hydrolysis of the oxidized B-chain of insulin by moose elastase was similar to that produced by porcine elastase with major cleavages occurring at Val-12-Glu-13, Ala-14-Leu-15 and Val-18-Cys(O-3H)-19 and minor cleavages occurring at Ser-9-His-10 and Arg-21-Gly-22. The hydrolysis of glucagon with moose elastase produced major cleavages at Thr-7-Ser-8, Ser-11-Lys-12, Val-23-Gln-24 and Leu-26-Met-27. The facile hydrolysis of Arg-17-Arg-18 was also observed and attributed, in part, to trypsin.
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PMID:Characterization of trypsin and elastase from the moose (Alces alces). I. Amino acid composition and specificity towards polypeptides. 112 77

To evaluate the role of hyperketonemia in the hypoalaninemia and decreased protein catabolism of prolonged starvation, Na dl-beta-hydroxybutyrate was administered as a primed continuous 3-6-h infusion in nonobese subjects and in obese subjects in the postabsorptive state and after 3 days and 3-5 1/2 wk of starvation. An additional obese group received 12-h ketone infusions on 2 consecutive days after 5-10 wk of fasting. The ketone infusion in nonobese and obese subjects studied in the postabsorptive state resulted in total blood ketone acid levels of 1.1-1.2 mM, a 5-15 mg/100 ml decrease in plasma glucose, and unchanged levels of insulin, glucagon, lactate, and pyruvate. Plasma alanine fell by 21% (P smaller than 0.001) in 3 h. In contrast, other amino acids were stable or varied by less than 10%. Infusions lasting 6 h reduced plasma alanine by 37%, reaching levels comparable to those observed in prolonged starvation. Equimolar infusions of NaC1 and/or administration of NaHCO3 failed to alter plasma alanine levels. During prolonged fasting, plasma alanine, which had fallen by 40% below prefast levels, fell an additional 30% in response to the ketone infusion. In association with repeated prolonged (12 h) infusions in subjects fasted 5-10 wk, urinary nitrogen excretion fell by 30%, returning to base line after cessation of theinfusions and paralleling the changes in plasma alanine. Ketone infusins resulted in two- to fourfold greater increments in blood ketone acids in fasted as compared to postabsorptive subjects. It is concluded that increased blood ketone acid levels induced by infusions of Na DL-beta-hydroxybutyrate result in hypoalaninemia and in nitrogen conservation in starvation. These data suggest that hyperketonemia may be a contributory factor in the decreased availability or circulating alanine and reduction in protein catabolism characteristic of prolonged fastings9
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PMID:Effect of ketone infusions on amino acid and nitrogen metabolism in man. 113 79

Although the stimulatory effect of glucagon on gluconeogenesis has been well demonstrated in certain systems in vitro, this effect has never been established in man. The present study was undertaken, therefore, to determine whether glucagon could stimulate gluconeogenesis from alanine in normal fasting man. Glucagon might stimulate this process by increasing the hepatic alanine uptake and/or by shunting the extracted alanine within the liver into the gluconeogenic pathway. In order to be able to examine these two aspects of gluconeogenesis, we combined the hepatic vein-brachial artery catheterization technic with an istopic infusion of alanine-14C. Alanine-14C specific activity was measured in whole blood and plasma by use of a rapid chromatographic technic. Since plasma contributed 93 per cent of the alanine extracted by the splanchnic bed with a specific activity three times that of the red blood cells, plasma alanine specific activity was used to study the conversion of alanine to glucose. A constant infusion of alanine-14C achieved a relatively stable arterial specific activity by forty minutes. The administration of glucagon by constant infusion (15-50 ng./kg./min.) had no affect on thf splanchnic extraction of alanine. Net splanchnic glucose-14C production, however, doubled during the glucagon infusion, and the conversion of alanine to glucose increased from 30 plus or minus 2 to 58 plus or minus 9 mumol/min. These data (1) demonstrate that in normal man fasted twelve to fourteen hours, glucagon at supraphysiologic levels can double the rate of gluconeogenesis from alanine and (2) indicate that this stimulatory effect of glucagon is exerted within the liver by shunting the extracted alanine toward new glucose formation rather than by increasing the hepatic extraction of alanine.
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PMID:Gluconeogenesis from alanine in normal postabsorptive man. Intrahepatic stimulatory effect of glucagon. 114 May 13


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