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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of glucose ingestion on the changes in blood glucose, FFA, insulin and glucagon levels induced by a prolonged exercise at about 50% of maximal oxygen uptake were investigated. Healthy volunteers were submitted to the following procedures: 1. a control test at rest consisting of the ingestion of 100 g glucose, 2. an exercise test without, or 3. with ingestion of 100 g of glucose. Exercise without glucose induced a progressive decrease in blood glucose and plasma insulin; plasma glucagon rose significantly from the 60th min onward (+45 pg/ml), the maximal increase being recorded during the 4th h of exercise (+135 pg/ml); plasma FFA rose significantly from the 60th min onward and reached their maximal values during the 4th h of exercise (2177 +/- 144 muEq/l, m +/- SE). Exercise with glucose ingestion blunted almost completely the normal insulin response to glucose. Under these conditions, exercise did not increase plasma glucagon before the 210th min; similarly, the exercise-induced increase in plasma FFA was markedly delayed and reduced by about 60%. It is suggested that glucose availability reduces exercise-induced glucagon secretion and, possibly consequently, FFA mobilization.
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PMID:Effect of glucose on plasma glucagon and free fatty acids during prolonged exercise. 67 44

We investigated the influence of an insulin-induced hypoglycemia on plasma glucagon in nonpregnant healthy young women and in women during the last month of gestation. Both groups were tested either in the basal state or during a period where free fatty acid plasma levels were increased by infusion of a lipid emulsion supplemented with heparin. Regular insulin was injected intravenously at the dose of 0.1 U/kg body wt in controls and 0.3 U/kg in pregnant women in order to obtain a similar lowering of blood glucose in all groups. In controls, the increase in plasma glucagon was maximum 30 and 45 min after insulin injection and averaged 130 pg/ml; the infusion of triglycerides and heparin which raised plasma FFA to about 1300 muEq/liter decreased basal plasma glucagon levels and reduced, by about 70%, the glucagon response to hypoglycemia. During the last month of pregnancy, the glucagon response to insulin-induced hypoglycemia was reduced by 60% (mean maximal increase 52 pg/ml); furthermore, raising plasma FFA to about 1500 muEq/liter completely abolished the glucagon rise induced by the insulin hypoglycemia. These results support the view that the glucagon release from A-cells can be modulated by the level of circulating plasma FFA.
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PMID:Influence of elevated plasma free fatty acids on the glucagon response to hypoglycemia in normal and in pregnant women. 68 68

Plasma FFA, glucagon, insulin, glucose, and growth hormone were followed every hour during 24 hours of saline infusion, 24 hours of somatostatin (4mg.) infusion, and three hours without infusion in six nonobese and six obese maturity-onset diabetic men. Somatostatin induced the same changes in the parameters of both groups of diabetic patients: A rise in plasma FFA, which gradually disappeared after some hours of infusion, a suppression of plasma glucagon and insulin, and an augmentation of plasma glucose both postprandially and during the night. Plasma growth hormone was suppressed in the nonobese patients, but somatostatin could not further suppress the low and nonfluctuating plasma growth hormone concentration in the obese maturity-onset diabetics. The results indicate that a preparation with a pattern of hormone suppression like that of somatostatin will not be useful in the control of maturity-onset diabetes, because it suppresses insulin and elevates the blood glucose concentration.
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PMID:Somatostatin in maturity-onset diabetes. 70 Feb 57

An investigation was carried out in conscious dogs concerning the effects of three adenosine derivatives substituted at the 5'-(744-96) or 2'-, 3'-, and 5'-positions (744-98, 744-99), with pronounced and long-lasting coronary dilator activity, on glucagon release. All three compounds (10 microgram/kg i.v.) induced a sustained increase in plasma glucose and a decrease in plasma FFA concentration; concomitantly, plasma glucagon levels rose 2--3 fold. Changes in plasma insulin concentration were relatively small and of no statistical significance. A simultaneous fall in arterial blood pressure was also observed. A lowering of blood pressure of similar magnitude by sodium nitroprusside infusion in control experiments failed to show any significant effect on plasma glucagon level. These results point to a specific effect of vasoactive adenosine derivatives on glucagon release.
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PMID:Evidence for glucagon-releasing activity of vasoactive adenosine analogues in the conscious dog. 71 81

The response of glucose, FFA and immunoreactive insulin to intravenous glucose and glucagon was examined in 6 apparently healthy subjects aged 67-77 years at 08(00) and 18(00) with a 3 day interval. The subjects, fasted 12 h before each test, received 0.5 g/kg of glucose i.v. and, 40 min after glucose, 1 mg glucagon i.v. The results confirmed, also in aged subjects, an impaired glucose tolerance in the afternoon test, as previously reported in the adult subject. The insulin response was delayed in the afternoon test, but the total incremental area was not significantly reduced. There was not a clearcut difference in the pattern of FFA response. The results could be a further confirmation of the central role of insulin response as a cause of impaired glucose tolerance in the afternoon also in subjects aged over 65 years.
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PMID:The response of glucose, insulin and FFA to intravenous glucose and glucagon in elderly subjects in the course of morning and afternoon tests. 74 86

To study the individual effects of glucagon and growth hormone on human carbohydrate and lipid metabolism, endogenous secretion of both hormones was simultaneously suppressed with somatostatin and physiologic circulating levels of one or the other hormone were reproduced by exogenous infusion. The interaction of these hormones with insulin was evaluated by performing these studies in juvenile-onset, insulin-deficient diabetic subjects both during infusion of insulin and after its withdrawal. Infusion of glucagon (1 ng/kg-min) during suppression of its endogenous secretion with somatostatin produced circulating hormone levels of approximately 200 pg/ml. When glucagon was infused along with insulin, plasma glucose levels rose from 94 +/- 8 to 126 +/- 12 mg/100 ml over 1 h (P less than 0.01); growth hormone, beta-hydroxy-butyrate, alanine, FFA, and glycerol levels did not change. When insulin was withdrawn, plasma glucose, beta-hydroxybutyrate, FFA, and glycerol all rose to higher levels (P less than 0.01) than those observed under similar conditions when somatostatin alone had been infused to suppress glucagon secretion. Thus, under appropriate conditions, physiologic levels of glucagon can stimulate lipolysis and cause hyperketonemia and hyperglycemia in man; insulin antagonizes the lipolytic and ketogenic effects of glucagon more effectively than the hyperglycemic effect. Infusion of growth hormone (1 mug/kg-h) during suppression of its endogenous secretion with somastostatin produced circulating hormone levels of approximately 6 ng/ml. When growth hormone was administered along with insulin, no effects were observed. After insulin was withdrawn, plasma beta-hydroxybutyrate, glycerol, and FFA all rose to higher levels (P less than 0.01) than those observed during infusion of somatostatin alone when growth hormone secretion was suppressed; no difference in plasma glucose, alanine, and glucagon levels was evident. Thus, under appropriate conditions, physiologic levels of growth hormone can augment lipolysis and ketonemia in man, but these actions are ordinarily not apparent in the presence of physiologic levels of insulin.
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PMID:Effects of physiologic levels of glucagon and growth hormone on human carbohydrate and lipid metabolism. Studies involving administration of exogenous hormone during suppression of endogenous hormone secretion with somatostatin. 82 Jul 17

Cyclic somatostatin was administered intravenously (10 mug/min for 60 min) to 10 healthy overnight fasted (postabsorptive) subjects and to 5 healthy 60-h fasted subjects. In both groups, arterial insulin and glucagon fell 50% and splanchnic release of these hormones was inhibited. In the overnight fasted subjects splanchnic glucose output fell 70%, splanchnic uptake of lactate and pyruvate was unchanged, alanine uptake fell by 25%, and glycerol uptake rose more than twofold in parallel with an increase in arterial glycerol. In the 60-h fasted group splanchnic glucose output was less than 40% of that observed in the overnight fasted subjects. Somatostatin led to a further decrease (--70%) in glucose production. Splanchnic uptake of lactate and pyruvate fell by 30-40%, amino acid uptake was unchanged, while uptake of glycerol rose fivefold. Total uptake of glucose precursors thus exceeded the simultaneous glucose output by more than 200%. Splanchnic uptake of FFA rose fourfold during somatostatin while output of beta-hydroxybutyrate increased by 75%. Estimated hepatic blood flow fell 25-35% and returned to base line as soon as the somatostatin infusion ended. It is concluded that (a) somatostatin-induced hypoglucagonemia results in inhibition of splanchnic glucose output in glycogen-depleted, 60-h fasted subjects as well as in postabsorptive subjects, indicating an effect of glucagon on hepatic gluconeogenesis as well as glycogenolysis; (b) the glucagonsensitive step(s) in gluconeogenesis affected by somatostatin involves primarily intra-hepatic disposal rather than net hepatic uptake of glucose precursors; (c) splanchnic uptake of fatty acids and ketone output are increased in the face of combined insulin and glucagon deficiency; and (d) diminished splanchnic blood flow may contribute to some of the effects of somatostatin on splanchnic metabolism.
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PMID:Influence of somatostatin on splanchnic glucose metabolism in postabsorptive and 60-hour fasted humans. 83 77

The responses to moderate exercise of circulating energy fuels and endocrine pancreatic hormones were examined in insulin-dependent diabetics receiving insulin either sc or by continuous iv infusion. Eight subjects received one-third of their usual daily insulin doses sc in the thigh 1 h prior to exercise. Seven subjects exercised during infusion (iv) of insulin at 8-20 mU"min, started 12-14 h earlier. Exercise was on a bicycle ergometer for 45 min at 50% maximum oxygen consumption. The diabetics receiving sc insulin showed a sharp decline in glycemia from elevated resting levels (227 +/- 16 mg/dl), in contrast to the control subjects whose glycemia did not change. The control subjects insulin (IRI) fell, and glucagon (IRG) remained unchanged. In the sc-insulin diabetics, exercise induced a further rise in IRG from elevated levels (296 +/- 76 pg/ml). Resting lactate, pyruvate and alanine were normal and increased as in controls. Though FFA, glycerol and ketone body levels were normal at rest, FFA failed to rise with exercise as in the controls and glycerol and ketone body increments were smaller. RQ increased and remained elevated in contrast to the later fall in controls during exercise. These results are consistent with selective insulin deficiency at rest, and increased insulin effect during exercise. This resulted in greater carbohydrate utilization during exercise, but without the normal shift back toward utilization of fat-derived fuels with continuation of exercise. Diabetics receiving insulin by infusion showed no glycemic change with exercise. Exercise caused greater increases in lactate and pyruvate levels (4-fold), although alanine levels increased only during recovery. The significantly elevated resting FFA levels showed a rise which was sustained at higher than control values during recovery; glycerol and ketone body increments also tended to be greater than in controls. Intravenous insulin sustained euglycemia in exercise, obviating the fall in glycemia with sc insulin. The responses of other metabolite levels were abnormal, and consistent with a subtle degree of underinsulinization.
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PMID:The metabolic response to moderate exercise in diabetic man receiving intravenous and subcutaneous insulin. 84 81

The in vivo effects of glucagon on the metabolism of extra-hepatic tissues have been investigated in eviscerated, functionally hepatectomized rats with intact kidneys. In these animals, even pharmacological amounts of exogenous glucagon did not significantly alter plasma glucose, FFA, or amino acids, compared with saline treatment. The possible secondary release of adrenal catecholamines following such doses of glucagon appeared to be similarly ineffective in increasing the peripheral tissue mobilization of substrates. It was only when the eviscerated animals were pretreated with insulin that the subsequent administration of glucagon or epinephrine elicited significant elevations in plasma FFA. The concomitant evisceration and adrenalectomy did not produce results which were significantly different from evisceration alone. Both kinds of animals required insulin pretreatment before a lipolytic response to glucagon or epinephrine could be demonstrated. This suggests that severe insulin insufficiency itself elicits almost maximum catabolism in these animals and that the further addition of other catabolic hormones such as glucagon or epinephrine cannot increase these catabolic effects, as manifest in plasma concentrations of FFA. These data show an extra-hepatic lipolytic effect of glucagon in vivo, but do not illuminate the significance of this effect in the intact animal.
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PMID:Studies on the extra-hepatic effects of glucagon in the eviscerated rat. 95 59

The study investigated the respective influences of nicotinic acid and somatostatin on plasma concentrations of blood glucose, free fatty acids, glucagon, growth hormone and cortisol in insulin-dependent diabetic subjects. After administration of nicotinic acid alone, marked depression of plasma FFA was accompanied by significant increases of plasma glucagon, growth hormone and cortisol. The glucagon and growth hormone responses to nicotinic acid were significantly reduced when plasma FFA were raised by intravenous administration of heparin and triglycerides. Somatostatin alone induced a significant decrease in blood glucose, plasma glucagon and growth hormone concentrations. Plasma FFA remained unchanged. Somatostatin did not modify the nicotinic acid-induced fall in plasma FFA, but completely blocked the corresponding increments in glucagon and growth hormone. The cortisol rise was not altered by somatostatin. Rebound of glucagon and growth hormone levels were seen upon discontinuation of the somatostatin administration. These results demonstrate that the plasma FFA concentration plays a role in the regulation of glucagon and growth hormone secretion in insulin-dependent diabetics. Furthermore, they indicate that somatostatin, previously shown to be capable of negating the stimulatory effect of various factors on glucagon and growth hormone secretion, also affects the response of these hormones to FFA depression.
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PMID:Effect of somatostatin on metabolic and hormonal changes induced by nicotinic acid in insulin-dependent diabetics. 97 35


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