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)

Healthy subjects were studied at rest and during 4 h of exercise at approximately 30% of maximal oxygen uptake. At 90 min of exercise 200 g glucose were ingested. A control group was studied during prolonged exercise without glucose administration. Glucose ingestion was followed by a 35% rise in arterial glucose, a 60-70% fall in arterial FFA and glycerol and a two- to threefold rise in arterial insulin. Plasma glucagon, which rose fourfold in controls, failed to rise in the glucose-fed subjects. Glucose uptake by the exercising legs was twofold greater than in controls, accounting for 60% of leg oxygen consumption. Splanchnic glucose output rose rapidly after glucose ingestion to values twice those observed in controls. However, splanchnic uptake of gluconeogenic precursors (lactate, pyruvate and glycerol) fell by 70-100%. Total splanchnic glucose escape after glucose ingestion was 84 +/- 5 g representing 42% of the ingested load. It is concluded that glucose ingestion during prolonged exercise results in a) augmented uptake and oxidation of glucose by the exercising legs, b) diminished lipolysis, c) augmented splanchnic glucose escape in association with decreased hepatic gluconeogenesis, d) retention of half of the ingested glucose within the splanchnic bed, and e) reversal of exercise-induced stimulation of glucagon secretion.
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PMID:Influence of glucose ingestion on fuel-hormone response during prolonged exercise. 99 55

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 response to glucagon infusion of blood glucose, blood lactate and plasma FFA was studied in 7 normoglycaemic and 7 hypoglycaemic SGA infants. The infants received glucagon at a rate of 0.2 microng/kg/min into a cephalic vein for a period of four hours. Glucagon caused a marked and significant rise in blood glucose in both groups; from 66 +/- 12 mg/100 ml to 136 +/- 16 mg/100 ml in the normoglycaemic, and from 22 +/- 2 mg/100 ml to 69 +/- 13 mg/100 ml in the hypoglycaemic infants. The time course of the response was different: while in the former group blood glucose declined after the second hour of glucagon infusion, in the hypoglycaemic group the response persisted throughout the test period. In the normoglycaemic SGA infants FFA fell rapidly in response to glucagon, whereas no significant change occurred in hypoglycaemic infants. The different baseline lactate concentrations were not affected significantly.
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PMID:The metabolic effects of glucagon infusion in normoglycaemic and hypoglycaemic small-for-gestational-age infants. I. Changes in blood glucose, blood lactate and plasma free fatty acids. 102 23

Animal experiments have suggested a FFA control mechanism for glucagon secretion. In man, the potent effect of FFA on HGH secretion and the similarity of the secretory control mechanisms for HGH and IRG also support a role of FFA in IRG secretion. Our studies in man in which plasma FFA were elevated by either an oral lipid emulsion (Lipomul) or an intravenous lipid suspension (Intralipid)suggest only a minor role of lipids in control of IRG secretion. Plasma FFA and triglyceride elevations did not suppress arginine- or hypoglycemia-induced plasma IRG elevations, but an inhibitory effect of Intralipid on basal plasma IRG concentrations was observed. Although nicotinic acid administration, which caused a depression in plasma FFA, did elevate plasma IRG, the IRG elevation was considered more likely a consequence of stress induced by the drug. The failure of lipids to inhibit IRG secretion at FFA concentrations inhibiting HGH secretion indicates a dissociation in the secretory control mechanisms of the two hormones.
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PMID:Effect of lipids on glucagon secretion in man. 111 Jun 25

Pancreatectomized dogs developed hypertriglyceridemia. This probably resulted from a lack of insulin rather than a lack of glucagon, as it did not develop either in pancreatectomized dogs maintained on insulin, or in dogs with all but the uncinate process of the pancreas removed. The increase in plasma triglycerides was preceded by a decrease in post-heparin lipolytic activity (PHLA) and an increase in FFA. As the hypertriglyceridemia developed in fasted dogs who had previously been on fat-free diets, the triglyceride fatty acids (TGFA) were nondietary. These endogenous TGFA originated from adipose tissue rather than from de novo synthesis. The composition of the lipoprotein TGFA was identical to that of adipose tissue. Furthermore, nicotinic acid blocked the FFA increase and the development of the hypertriglyceridemia. However, it did not prevent the fall of PHLA. Although their TGFA were entirely nondietary, the lipoproteins in these diabetic dogs resembled chylomicrons in their electrophoretic mobility, size, density, and composition. Surgical, histological and tracer studies suggested that in addition to the liver, the intestinal mucosa makes these lipoproteins. The tracer studies also suggested that circulating FFA might enter the intestinal mucosal cells directly and be esterified.
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PMID:Production of chylomicron-like lipoproteins from endogenous lipid by the intestine and liver of diabetic dogs. 111 49

The influence of exercise on leg and splanchnic exchange of substrates was examined in eight insulin-dependent diabetics 24 h after withdrawal of insulin and in eight healthy controls studied at rest and after 40 min of bicycle ergometer exercise at 55-60% of maximal capacity. In four of the diabetic subjects, basal arterial ketone acid levels were 3-4 mmol/ liter (ketotic diabetics) and in the remainder, below 1 mmol/liter (nonketotic diabetics). ,ree fatty acid (FFA) turnover and regional exchange were evaluated with 14-C- labeled oleic acid. Leg uptake of blood glucose rose 13-18 fold during exercise in both the diabetics and controls and accounted for a similar proportion of the total oxygen uptake by leg muscles (25-28%) in the two groups. In contrast, leg uptake of FFA corresponded to 39% of leg oxygen consumption in the diabetic group but only 27% in controls. Systemic turnover of oleic acid was similar in the two groups. Splanchnic glucose output increased during exercise 3-4 fold above resting levels in both groups. In the diabetics, splanchnic uptake of lactate, pyruvate, glycerol, and glycogenic amino acids rose more than twofold above resting levels and was fourfold greater than in exercising controls. Total precursor uptake could account for 30% of the splanchnic glucose output in the diabetic group. In contrast, in the controls, total splanchnic uptake of glucose precursors was no greater during exercise than in the resting state and could account for no more than 11% of splanchnic glucose output. The augmented precursor uptake during exercise in the diabetics was a consequence of increased splanchnic fractional extraction as well as increased peripheral production of gluconeogenic substrates. The arterial glucagon concentration was unchanged by exercise in both groups, but was higher in the diabetics. In the diabetic subjects with ketosis in the resting state, exercise elicited a rise in arterial glucose and FFA, an augmented splanchnic uptake of FFA, and a 2-3 fold increase in splanchnic output of 3-hydroxybutyrate. Uptake of 3-hydroxybutyrate by the exercising leg rose more rapidly than splanchnic production, resulting in a fall in arterial levels of 3-hydroxybutyrate. It is concluded that (a) glucose uptake by exercising muscle in hyperglycemic diabetics is no different from that of controls; (b) splanchnic glucose output rises during exercise to a similar extent in diabetics and controls, while uptake of gluconeogenic substrates is markedly higher in diabetics and accounts for a greater proportion of total splanchnic glucose output; (c) exercise in diabetic patients with mild ketosis is associated with a rise in blood glucose and FFA levels as well as augmented splanchnic production and peripheral uptake of ketone bodies.
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PMID:Splanchnic and leg exchange of glucose, amino acids, and free fatty acids during exercise in diabetes mellitus. 113 76

The lipolytic effect of glucagon was measured in vitro with adipose tissue of "young" (4-8 wk) and "old" (over 1 yr) geese. The response of the young geese tissue was about twice that observed with tissue of old geese, for glucagon concentrations of 0.05, 0.5, and 5.0 mug/ml. Our estimates indicate that the number of adipose cells per g of adipose tissue of young geese was three times that of the old geese tissue. This suggests that the greater lipolytic response to glucagon, observed in young geese adipose tissue, may possibly be due to its greater cellularity, rather than to a greater lipolytic response of the individual adipocyte. The lipolytic effect of glucagon in vivo, for each of the doses between 1.0 and 20.0 mug/kg, was significantly greater in the old than in the young geese. The slope of the linear equation relating log10 of glucagon dose and elevation of plasma FFA 5 min after injection, was significantly greater for the old than for the young geese. In the goose, therefore, the influence of age on the adipokinetic effect of glucagon appears to be mediated by factors operating in the whole animal, more than by changes in the adipose cell itself. A slower removal rate of circulating FFA by the old geese, could be one of these factors.
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PMID:Age influence on the lipolytic effect of glucagon in geese. 114 55

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

Significant increases in mean plasma noradrenaline levels were observed 30-60 min and 150-180 min after a subcutaneous injection of 1 mg glucagon. The first peak coincided with the maximum blood glucose and plasma insulin levels and the second peak occurred after plasma growth hormone (GH) and cortisol levels had begun to rise. The first plasma noradrenaline peak may be important in inhibiting further insulin secretion. There was no evidence that glucagon stimulates adrenaline secretion in normal human subjects. It was also confirmed that there are significant increases in the levels of glucose, insulin, GH and cortisol and a significant decrease in FFA levels following subcutaneous injection of glucagon in normal human subjects.
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PMID:The metabolic and hormonal response to glucagon. Part 1. Normal subjects. 126 1

Cold acclimatization in rats at 5 degrees C for 2 weeks caused a significant elevation of plasma glucagon concentration, accompanied by increased plasma FFA and glucose levels. Acute cold exposure at 5 degrees C for 5 or 60 min did not affect these parameters in plasma.
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PMID:Is glucagon involved in cold acclimatization? 126 50


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