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)

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 alpha-ketoanalogues of the branched-chain amino acids were administered to fasting subjects to determine whether or not they promoted nitrogen sparing. Two fasting studies were carried out in each subject. During the first week of one of the two fasts 4.7 g of a mixture of the alpha-ketoanalogues of valine, leucine, and isoleucine were infused daily. No infusions were administered during the other fast, which served as a control. Urinary urea and calculated total urinary nitrogen were significantly lower during both the week of infusions and the ensuing week of fasting after the infusions were discontinued. Immediately after ketoacid infusions, plasma branched-chain amino acids, including allosioleucine, rose, while alanine and several other amino acids (but not glutamine) fell. There were no differences between the two fasts with respect to ketone bodies, free fatty acids, glucose, insulin, or glucagon concentrations. We conclude that branched-chain ketoacids spare nitrogen early in fasting and that this effect persists after they are metabolized.
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PMID:Nitrogen sparing induced early in starvation by infusion of branched-chain ketoacids. 83 56

In order to investigate the contribution of glucagon to the abnormalities of carbohydrate and lipid metabolism in diabetes, hormones and metabolites were measured in response to IV arginine in 5 juvenile onset (control) diabetics and 5 totally pancreatectomised subjects. In the basal state, both control diabetics and pancreatectomised patients showed abnormally elevated levels of plasma glucose, blood 3-hydroxybutyrate, glycerol and plasma free fatty acids (NEFA), although no glucagon was detectable in the plasma of the pancreatectomised subjects. Blood concentrations of the gluconeogenic precursors alanine and glycerol were higher pancreatectomised patients than in the diabetics. Following infusion of arginine, the rise in glucagon observed in the diabetics was accompanied by a significant increase in plasma glucose and a fall in blood lactate when compared to the pancreatectomised subjects. In spite of the rise in glucagon in the control diabetics, no sigficant change was found in the concentrations of ketone bodies, glycerol or NEFA. Thus glucagon does not seem to have a primary role in producing the metabolic abnormalities of diabetes.
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PMID:Persistent metabolic abnormalities in diabetes in the absence of glucagon. 83 5

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 hormonal and metabolic response to the first feed of breast milk was studied in 12 infants at 4-6 hours of age. After the feed there was an increase in blood glucose concentration but no changes in the concentrations of lactate, pyruvate, alanine, or ketone bodies. The feed was followed by an increase in the concentrations of plasma insulin, growth hormone, gastrin, and enteroglucagon, but no change in levels of plasma glucagon or gastric inhibitory peptide. Several hormone systems are functionally active at birth and are stimulated by the first feed of milk.
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PMID:Endocrine and metabolic response in the human newborn to first feed of breast milk. 86 Aug 74

Seven men ran at 60% of individual maximal oxygen uptake to exhaustion during beta-adrenergic blockade with propranolol or without drugs. After propranolol administration the increases during exercise in plasma glucagon and epinephrine concentrations as well as the decrease in plasma glucose concentrations were faster than in control experiments. When euglycemia was maintained by glucose infusion during beta-adrenergic blockade, glucagon and epinephrine responses to exercise, although not abolished, were markedly reduced. The diminution of the exercise-induced decline in glucose concentrations correlated significantly with the diminution of the glucagon as well as the epinephrine responses. Thus decreased glucose concentrations may significantly enhance the secretion of glucagon and epinephrine during prolonged exercise in man. Since the diminution of the glucagon response produced by glucose infusion was not accompanied by significant alterations in the levels of nonesterified fatty acid (NEFA) and glycerol, increased glucagon secretion does not seem to be a major determinant of lipolysis during exercise in man. During glucose infusion, glycogen utilization rates in muscle (n = 4) tended to decrease, whereas carbohydrate combustion rate and concentrations of norepinephrine, insulin, alanine, and lactate were unchanged.
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PMID:Glucose-induced decrease in glucagon and pinephrine responses to exercise in man. 86 12

Hormonal and metabolic effects of a synthetic linear somatostatin were tested in insulin-dependent subjects submitted to an intravenous arginine infusion. Arginine alone induced a rise in plasma growth hormone (HGH) and glucagon (IRG) concentrations but did not affect the spontaneous diurnal decrease of plasma cortisol; blood glucose concentration rose while that of alanine decreased suggesting enhanced gluconeogenesis; concentrations of plasma free fatty acids (FFA) and 3-hydroxybutyrate decreased. Somatostatin, at three different dosages, markedly influenced these patterns: HGH response to arginine was suppressed by the lowest somatostatin dose; IRG response was progressively inhibited by increasing doses of somatostatin but never reached zero; cortisol level was not decreased but slightly increased by somatostatin. Substrate responses to arginine were also modified by somatostatin: alanine disappearance was impaired, this effect being dose-related; plasma FFA and 3-hydroxybutyrate concentrations showed a significant increase rather than decrease, consistent with somatostatin suppression of residual insulin secretion. Tolerance to somatostatin was good and no alteration of hemostasis was observed.
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PMID:Hormonal and metabolic effects of somatostatin in diabetic patients submitted to an i.v. arginine infusion. 87 Mar 53

To determine the fetal response to altered maternal fuel supply, the effects of prolonged maternal fasting, begun 24-96 h before term, were examined and compared with values from normally fed term animals. Fetal weight decreased only after 48 h of maternal fasting. Prolonged maternal fasting was associated with low blood glucose, high blood ketone bodies, and decreased gluconeogenic substrate in the fetus. Plasma insulin was decreased, whereas plasma glucagon was increased in the fetus of fasted mothers. Infusion of [2-3H]glucose into the mother to constant specific activity gave a ratio of maternal to fetal glucose activity of 1.0 in fed and 1.56 in fasted mothers. Fetal liver from fasted mothers showed both increase in activity of key gluconeogenic enzymes (glucose-6-phosphatase and phosphoenolpyruvate carboxykinase) and increased conversion in vitro of lactate, alanine, serine, and glycerol in glucose by liver slices. It is inferred that maternal fasting induces fetal substrate alterations and hormonal changes appropriate to premature appearance of hepatic gluconeogenesis. The priority for endogenous fuel provision in this state leads to impaired fetal growth.
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PMID:Fetal metabolic response to maternal fasting in the rat. 87 Nov 55

1. The injection of L-alanine (50-100 mg/kg) into 35-day-old rats that had been starveed for 48 h increased blood L-alanine concentration to values observed in fed animals and lowered the blood concentration of 3-hydroxybutyrate within 2 min. 2. This hypoketon aemic action of L-alanine was specific for 3-hydroxybutyrate, since the acetoacetate concentrations did not change significantly. 3. The decrease in 3-hydroxybutyrate elicited by L-alanine was not related to changes in the blood concentrations of insulin, glucagon, growth hormone, glucose, unesterified fatty acids, lactate or pyruvate. 4. The injection of L-alanine resulted in a decrease in total ketones that was apparently unrelated to their increased peripheral utilization. These results are interpreted as an anti-ketogenic action of L-alanine. 5. The data suggest that L-alamine lowers ketone-body formation in starved rats, possibly via an alteration in hepatic redox equilibrium.
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PMID:Hypoketonaemic effect of L-alamine. Specific decrease in blood concentrations of 3-hydroxybutyrate in the rat. 88 51

Alanine (500 mg/kg body weight) was given orally to 27 healthy full term newborn infants, and the changes in blood glucose, pyruvate, lactate, alanine, glucagon and insulin were determined. Significant increments in blood glucose were found in 15 infants with blood glucose levels below 60 mg/100 ml, 4 of whom showed significant elevation of serum glucagon levels on day 1. This observation suggests that hepatic gluconeogenesis is possible immediately after birth.
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PMID:The effects of oral alanine administration on blood glucose, pyruvate, lactate, serum glucagon and insulin in human newborns. 88 46


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