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)

The metabolic responses to 4-h infusions of adrenaline (3 micrograms kg-1 h-1) and cortisol (10 mg m-2 h-1 for 2 h followed by 5 mg m-2 h-1 for 2 h), separately and in combination, have been studied in six healthy subjects with concurrent somatostatin infusion (250 micrograms h-1). A combined infusion of adrenaline, cortisol, glucagon (180 ng kg-1 h-1) and somatostatin has also been studied. Somatostatin plus adrenaline and somatostatin plus cortisol resulted in hyperglycaemia (at 240 min, somatostatin plus adrenaline 11.4 +/- 0.4 mmol l-1, P less than 0.001; somatostatin plus cortisol 6.7 +/- 0.3 mmol l-1, P less than 0.05; somatostatin alone 4.9 +/- 0.4 mmol l-1). No synergistic effect on blood glucose was seen with adrenaline and cortisol together. When glucagon was added, blood glucose rose more rapidly than without glucagon (9.3 +/- 0.4 mmol l-1 v. 7.2 +/- 0.5 mmol l-1 at 45 min, P less than 0.001), but plateau values were similar. Plasma NEFA levels were raised by somatostatin plus adrenaline (0.55 +/- 0.04-1.82 +/- 0.11 mmol l-1 at 60 min). Somatostatin plus cortisol had no more effect on plasma NEFA than somatostatin alone. During the combined infusion of somatostatin plus adrenaline plus cortisol, a synergistic effect on plasma NEFA was observed (2.30 +/- 0.11 mmol l-1 at 60 min, P less than 0.01 v. somatostatin plus adrenaline). This occurred despite a small escape of insulin secretion. The lipolytic actions of adrenaline are potentiated by elevated circulating cortisol levels in insulin-deficient man.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interactions of stress hormones on lipid and carbohydrate metabolism in man with partial insulin deficiency. 287 80

In order to find out the influence of hyperinsulinaemia and initial blood glucose levels on glucose homeostasis during physical exercise, 6 Type 2 diabetic patients with basal hyperinsulinemia (0.209 nmol/l) (group A) and 10 Type 2 diabetics without basal hyperinsulinemia (0.046 nmol/l) (group B) took part in a study on metabolic effects of exercise. Mean bodymass was higher in group A (101 kg) than in group B (71.7 kg). Exercise was performed on a bicycle-ergometer for 1 hr. Work load was adjusted to a pulse-rate of 120/min with a mean of 48 watt (W) in group A and 52 W in group B. Blood glucose (BG), insulin (IRI), glucagon (G), growth hormone (HGH), cortisol (C), epinephrine (E), norepinephrine (NE), lactate (L), pyruvate (P) and free fatty acids (NEFA) were measured during 3 hr. BG and IRI were also documented for the following 7 hr. Both groups showed a small but significant decrease of BG during exercise (group A from 11.54-10.38 mmol/l, p less than 0.01, and group B from 8.71-7.22 mmol/l, p less than 0.005). IRI decreased insignificantly in group A (from 0.209-0.174 nmol/l, p less than 0.15) and significantly in group B (from 0.046-0.032 nmol/l, p less than 0.01). G increased significantly in both groups (from 62.4-75.2 pmol/l in A, p less than 0.05, and from 38.8-47.1 pmol/l in B, p less than 0.01). HGH rose from 0.018-0.149 nmol/l in A, p less than 0.01, and from 0.077-0.320 nmol/l in B, p less than 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hormonal and metabolic response to physical exercise in hyperinsulinemic and non-hyperinsulinemic type 2 diabetics. 355 53

The effects of a high-fat diet on ketonemia and other plasma parameters of gluconeogenesis and ketogenesis were studied in rabbits during feeding, during a 4-day fast, and again during refeeding. Arterial plasma glucose, lactate, total aminoacids, ketone bodies, insulin and glucagon were measured daily. In the fed state, the high-fat diet induced an increase in plasma NEFA and ketone bodies and a decrease in alaninemia. The most striking effect of the high-fat diet, compared with the normal low-fat diet was the twofold increase of ketonemia during fasting, even though the difference in NEFA level after both diets was only 19%. This effect was maintained throughout the fasting period. The high-fat diet also induced higher glycemia and lower alaninemia during further fasting. Insulinemia sharply decreased to a very low value from the beginning of fasting, but the high-fat diet did not have any particular effect. Glucagonemia was not different in the fed state than in fasting, whatever preceding diet was given. Therefore, lipid content of the diet prior to fasting introduced important and persistent modifications in the triglycerides and glucose metabolism during fasting.
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PMID:Effects of dietary lipid level on ketonemia and other plasma parameters related to glucose and fatty acid metabolism in the rabbit during fasting. 389 42

One group of 10 obese people (1.72 times normal weight) was compared to a control group of 9 normal-weight subjects. Oxygen consumption (VO2), immuno reactive growth hormone (IRGH), and rectal temperature (Tre) were measured every 15 min on an average, during the 5 h following a protein meal composed of 6 egg-whites and 50 g of casein totaling 1 340 kJ. The results show that postprandial thermogenesis (PPT) is the same in both groups: maximum increase in VO2 averages 15% in the obese and 16% in the control groups respectively. Energy expenditure integrated over the 5 h was 129 kJ for the obese and 114 kJ for the control subjects, i.e. 9.6% and 8.5% of the energy meal content. The rise in Tre was identical for both groups (0.4 degrees C over 3 h). For IRGH, the preprandial reference figures were much lower in the obese: 52 pmole.dm-3, as compared to 145 pmole.dm-3. In all control subjects, the protein meal resulted in a IRGH peak of, on average, 455 pmole.dm-3 about 2 h after. This was not observed in 4 of the obese subjects, while in the remaining 6, the mean peak value was 165 pmole.dm-3, occurring after 1 h. The other hormonal or chemical compound simultaneously analysed (glucagon, cortisol, PRL, T3, glucose, lactate, NEFA) do not show any significant variations but insulin blood level for which a postprandial increase was measured in both groups. It is concluded that after a protein test meal: PPT in overweight people is no different from that in people of normal weight.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postprandial thermogenesis and hormonal release in lean and obese subjects. 391 63

The aim of this study was to evaluate the metabolic effects of a new synthetic ACTH analogue (ACTH 1-17) in insulin-dependent diabetic subjects. ACTH 1-17 (100 micrograms, intramuscular injection) was administered at 07(00)-07(30) every second day for 20 days. Changes in insulin dosage were carried out to maintain the same metabolic control during the period of the study. Before and after treatment diurnal plasma glucose profiles were superimposable and insulin requirement increased only in 16 out of 19 patients (mean: 6.7 +/- 2 U/die; range: 2-22 U/die). No changes were observed in diurnal profiles of blood alanine, glycerol, total ketone bodies and plasma NEFA, C-peptide, glucagon. The physiological blood lactate and pyruvate peaks following the evening meal were initially absent and could be detected after treatment. From our data it is not clear whether the more physiological pattern of blood lactate and pyruvate is caused by the modest increase in insulin dosage or is a specific effect of the treatment.
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PMID:ACTH 1-17 effects in insulin dependent diabetes mellitus. 609 Dec 42

Some acute and chronic metabolic effects of a new ACTH analogue (ACTH 1-17, Synchrodyn) were evaluated in healthy subjects and compared to those of the synthetic fragment ACTH 1-24. The peptides were injected at doses reportedly comparable with regard to their corticotropic effect, i.e. 100 micrograms ACTH 1-17 and 250 micrograms ACTH 1-24. A similar increase in blood glucose, NEFA and ketone bodies concentrations, without any significant modification of insulin, C-peptide and glucagon levels, was observed after injecting both peptides. The chronic treatment with ACTH 1-24 induced a significant increase in basal lactate, pyruvate and alanine blood concentrations. The levels of these metabolites resulted unaffected or slightly reduced after the corresponding treatment with ACTH 1-17. Our data are compatible with a certain degree of exhaustion of the adrenocortical reserve or, alternatively, a resetting of the circadian cortisol rhythm after prolonged treatment with the ACTH 1-17 analogue.
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PMID:ACTH 1-17 effects on intermediary metabolites in healthy subjects. 609 Dec 41

In a double-blind randomized study, the effect of the acute administration of a single oral dose of oxprenolol, a nonselective beta-blocker, and of metoprolol, a beta 1 selective blocker, on insulin-induced hypoglycemia was tested in seven normal subjects. Neither of the drugs potentiated the hypoglycemic effect of insulin. The recovery from hypoglycemia was delayed by both blocking agents only in the late phases of the experimental observation. This effect could not be accounted for by suppression of release of the counterregulatory hormones glucagon or cortisol, but may be mediated by the inhibition of NEFA and gluconeogenic-substrate release in response to hypoglycemia. Both drugs blocked the hypoglycemia-induced tachycardia. Only oxprenolol raised diastolic blood pressure during hypoglycemia. Symptoms of hypoglycemia were not masked by either blocking agent, and sweating was enhanced and prolonged by both drugs. Thus, no clear-cut differences in the glycemic response to insulin-induced hypoglycemia were found between metoprolol and oxprenolol, but the drugs differed in their influence upon the blood pressure response to insulin-induced hypoglycemia.
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PMID:Beta blockade and diabetes mellitus: effect of oxprenolol and metoprolol on the metabolic, cardiovascular, and hormonal response to insulin-induced hypoglycemia in normal subjects. 610 48

The effect of the administration of a single oral dose of placebo, oxprenolol and metoprolol on insulin-induced hypoglycemia was investigated in seven insulin-dependent diabetics in a double-blind randomized study. Neither of the beta-blocking agents accelerated the plasma glucose lowering effect of insulin. Plasma glucose recovery from hypoglycemia was grossly impaired in diabetics whether blocked or not, and all investigations had to be terminated by i.v. glucose injection after 1 hr of sustained hypoglycemia. During the period of observation, no further delaying effect by either beta-blocker was observed. The lack of plasma glucose recovery seems to be at least in part related to a retarded and reduced glucagon response to hypoglycemia. Both drugs blocked the hypoglycemia-induced pulse rate increase, but neither caused bradycardia. A significant increase in diastolic pressure was recorded with oxprenolol, whereas a drop in systolic pressure was noted with metoprolol. Oxprenolol suppressed the NEFA rise after insulin-infusion termination to a greater extent than did metoprolol. Hypoglycemic symptoms were not affected by beta-blockade. The results suggest that neither drug further worsens the already grossly impaired plasma glucose recovery, but that oxprenolol and metoprolol may differ in their effects on hemodynamic response to hypoglycemia. This aspect of the problem requires further study under careful control in hypertensive diabetics.
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PMID:Beta blockade and diabetes mellitus: effect of oxprenolol and metoprolol on the metabolic, cardiovascular, and hormonal response to insulin-induced hypoglycemia in insulin-dependent diabetics. 610 49

The metabolic response to pathophysiologic concentrations of glucagon, induced by glucagon infusion, has been examined in normal man before and after 36-60 hr hypercortisolaemia, induced by administration of tetracosactrin-depot. Glucagon alone increased serum insulin levels twofold but blood glucose was unaltered. Plasma NEFA and blood ketone body concentrations were decreased by glucagon infusion. Tetracosactrin produced a threefold rise in serum cortisol levels and caused mild fasting hyperglycemia and hyperinsulinaemia. Subsequent glucagon infusion had no effect on circulating insulin, glucose, NEFA or ketone body concentrations. Simultaneous infusion of somatostatin, to produce partial insulin-deficiency, unmasked a hyperglycemic action of glucagon (+ 3.8 +/- 0.2 mmol/l at 90 min, p less than 0.02). This glucagon-induced rise in blood glucose was diminished by prior tetracosactrin administration. Tetracosactrin revealed a mild lipolytic action of glucagon in partial insulin deficiency, not apparent in the euadrenal state. Glucagon was equally hyperketonemic during somatostatin infusion before and after tetracosactrin. Thus the hyperglycemic and hyperketonemic actions of glucagon at pathophysiologic levels are restricted to insulin deficiency. Hypercortisolaemia reveals a lipolytic action of glucagon in insulin-deficient man but does not potentiate the hyperglycemic or hyperketonemic effects.
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PMID:Metabolic interactions of glucagon and cortisol in man--studies with somatostatin. 612 61

The metabolic effects of chronic hypercortisolaemia were studied by administration of tetracosactrin-depot, 1 mg I.M. daily for 36-60 hr to normal subjects. Partial insulin and glucagon deficiency were induced at the end of the period by infusion of somatostatin, 100 micrograms/h for 210 min. Tetracosactrin alone induced a three fold rise in basal serum cortisol levels and fasting blood glucose concentration rose from 5.2 +/- 0.2 to 7.2 +/- 0.2 mmole/l (p less than 0.01) with a rise in fasting serum insulin from 5.2 +/- 1.2 to 13.1 +/- 1.9 mU/l (p less than 0.02). Concentrations of the gluconeogenic precursors lactate, pyruvate and alanine were also raised, but non-esterified fatty acid, glycerol and ketone body levels were unchanged. Somatostatin infusion caused a 30%-50% decrease in serum insulin and a 20%-60% decrease in plasma glucagon concentrations both before and after tetracosactrin administration. A similar rise in blood glucose concentration, relative to the saline control, occurred over the period of somatostatin infusion both with and without elevated cortisol levels. However, prior tetracosactrin administration caused a 100% greater rise in blood ketone body concentrations during infusion of somatostatin than was seen in the euadrenal state, despite similar plasma NEFA concentrations. Hypercortisolaemia causes hyperglycaemia and elevated gluconeogenic precursor concentrations but the associated rise in serum insulin concentrations limits lipolysis and ketosis. In insulin deficiency, a ketotic effort of glucocorticoid excess is evident which may be independent of lipolysis and occurs despite concurrent glucagon deficiency. These catabolic actions of cortisol are likely to be of major importance in the metabolic response to stress.
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PMID:Metabolic effects of cortisol in man--studies with somatostatin. 612 62


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