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)

Total and mucosal blood flow in the nonsecreting stomach and the interrelation between local blood flow changes and gastric hydrochloric acid secretion as influenced by various drugs or hormones were investigated in 188 anaesthetized dogs. Substances acting on gastric acid secretion (histamine, pentagastrin, atropine and metiamide) and those showing vasoactive properties (norepinephrine, epinephrine, Hypertensin, nicotinic acid and glucagon) were used. Instillation of 0.1 N HCl solution into the stomach provided a good estimate of the mucosal blood flow of the nonsecreting stomach as measured by the aminopyrine clearance technique of Jacobson et al. Simultaneous recording of the total gastric blood flow with an electromagnetic blood flowmeter revealed the distribution of blood flowing through the mucosal and non-mucosal (submucosa-muscle) tissues of the resting stomach. During acid stimulation a shift of the gastric blood flow to the mucosa was observed, which may reach even 75--80% of the total amount of the blood supply during a given period. Metiamide entirely inhibited the gastric acid secretion induced by both histamine and pentagastrin, but did not parallelly diminish mucosal blood flow. Given during histamine infusion, glucagon strongly inhibited acid secretion while it did not decrease mucosal blood flow.
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PMID:Interrelation between gastric blood flow and HCl secretion in dogs. The basal condition and influence of secretory stimulants and vasoactive substances. 3 17

The effects of intravenous administration of isoprenaline, glucagon and nicotinic acid on plasma concentrations of cyclic AMP in rats are described. In order to determine the relative importance of the liver as a source of extracellular cyclic AMP, the effects of the hormones were investigated in intact and functionally hepatectomised rats. The results showed that hepatectomy did not prevent an isoprenaline-stimulated increase in plasma cyclic AMP concentrations, although glucagon was without effect on plasma nucleotide concentrations in this group of animals. It is suggested that the liver is essential for the action of glucagon but that isoprenaline can increase plasma cyclic AMP concentrations in hepatectomised animals by increasing extrahepatic release of the nucleotide. Since inhibition of adipose tissue lipolysis with nicotinic acid did not prevent an isoprenaline or glucagon-stimulated increase in plasma cyclic AMP concentrations, adipose tissue is discounted as a major source of plasma cyclic AMP.
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PMID:The sources of plasma cyclic AMP: studies in the rat using isoprenaline, nicotinic acid and glucagon. 16 83

The calorigenic action of glucagon was studied in several species by measuring its effect on the oxygen comsumption. The calorigenic effect was most pronounced in the quail and also evident in young adult rats of two different strains but not in mice and guinea pigs. The influence of various drugs on the calorigenic effect of glucagon was investigated in rats. Ganglionic blocking agents (hexamethonium, mecamylamine, chlorisondamine) as well as adrenergic blocking drugs (propranolol, butoxamine, phentolamine) greatly reduced the glucagon-induced calorigenesis but after pretreatment with reserpine, guanethidine or chemical sympathectomy with 6-hydroxydopamine the calorigenic effect of glucagon was exaggerated. It was somewhat diminished by nicotinic acid but not by chlorpromazine or lithium and potentiated by cocaine but not by theophylline.--These results are not indicative for an involvement of adenly cyclase--cyclic AMP--system in glucagon-induced calorigenesis but they are compatible with the assumption that the hormone enhances the metabolic rate by releasing catecholamines from the adrenal medulla.
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PMID:[The calorigenic effect of glucagon]. 24 4

A comparisonwas made of lipid circulation, storage, and mobilization in rats adapted to lard or glucose diets. In the morning, lard-fed rats had higher blood triglyceride (TG) and free fatty acid (FFA) levels. In the evening TG was higher, but FFA was significantly lower in the lard vs. the glucose group. Fasting did not produce the characteristic increase in blood FFA in the lard-fed rats but was associated with a severe drop in their serum TG. Circulating glucose and insulin were not affected, while glucagon levels were increased by lard feeding. Nicotinic acid decreased fasting FFA levels to a greater extent in the glucose-fed rats. It was concluded that lard feeding depresses mobilization of fat from adipose tissue; on the other hand, it was found to increase storage and utilization of muscle TG. Fat feeding increased diaphragm TG concentrations threefold, as well as the number and size of intracellular fat droplets at the light and electron microscopic levels. Fasting decreased diaphragm TG in both groups, but the amount lost was greater in the fat-fed rats. Also, in vitro basal isoproterenol-stimulated (1 microgram/ml) FFA release by the incubated diaphragm was higher in the lard-fed group.
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PMID:Studies on serum lipids, insulin, and glucagon and on muscle triglyceride in rats adapted to high-fat and high-carbohydrate diets. 65 83

This study was designed to evaluate the metabolic response to limitation of fat mobilization during severe exercise in man. To this end, we assessed the relationship between fat mobilization, lipid-ketone physiology, and exercise-induced elevations in the counter-regulatory hormones. Ten well trained athletes ran a 10-mile premeasured course in as short a time as possible during both a placebo and an experimental study. In the experimental study, fat mobilization was inhibited by the oral administration of 2 g of nicotinic acid. Blood samples for multiple substrate and hormonal assay were obtained 2 h before exercise, immediately before exercise, and immediately after exercise. In the experimental study, nicotinic acid effectively blocked the expected rise in plasma free fatty acid concentration observed in the placebo study. Although blunted, the exercise-induced rise in plasma ketone concentration persisted in spite of the reduced free fatty acid levels. The significance of the concommitant exagerated rise in glucagon and GH in stimulating ketogenesis is discussed. The inhibition of fat mobilization did not reduce the mean time required to run 10 miles. Since muscle uptake of free fatty acid is directly proportional to the plasma concentration of this substrate, our study suggests that the inability to mobilize fat does not prevent severe exercise for 70 min.
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PMID:Effects of altered free fatty acid mobilization on the metabolic response to exercise. 75 Jun 3

Carbohydrate metabolism is temporarily disturbed in acute myocardial infarction. The degree of hyperglycaemia and failure of response of insulin appears to be related to the severity of the infarction. The underlying hormonal changes probably include increased secretion of catecholamines and of glucagon. Circulating free fatty acids (FFA) are generally increased by the same metabolic and hormonal factors which promote glucose intolerance. In the zone of developing infarction in the heart, there is a complex metabolic situation with glucose metabolism both being accelerated and inhibited by different factors. Continued uptake of FFA is associated with intracellular accumulation of activated long-chain FFA, acyl CoA, which tends to inhibit mitochondrial metabolism. The metabolism of glucose is thought to be beneficial and that of FFA detrimental to the infarcting tissue. Thus the glucose intolerance and the high circulating FFA occurring as part of the general metabolic response to myocardial infarction, are thought to be harmful to the ischaemic tissue. Increased provision of glucose by dichloroacetate, and inhibition of FFA metabolism by nicotinic acid analogues decrease the extent of experimental infaraction, while glucose--insulin--potassium and propranolol act both by increasing glucose uptake and decreasing that of FFA. Glucose intolerance is also common in peripheral vascular disease. The reasons for this are obscure. However, the alterations in circulating insulin concentration which accompany this intolerance may be involved in the development of arterial lesions either directly through an effect on arterial wall synthesis or indirectly through an effect on circulating lipid levels. Defects may also be found in arterial wall mucopolysaccharide or sorbitol metabolism. The role of sex hormones and catecholamines remains speculative. At present the most cogent view is that in peripheral vascular disease a multi-hormonal disorder exists which may be contributing to the development of arteriosclerosis.
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PMID:Carbohydrate metabolism in cardiovascular disease. 79 85

It has previously been shown that nicotinic acid (NA)-induced depression of free fatty acids (FFA) stimulates the secretion of GH and glucagon. To evaluate this hormonal response further, we studied the influence of different doses of glucose administered by continuous iv infusion on the GH and glucagon increase during NA-induced FFA depression. In ten male non-obese volunteers, FFA depression by the infusion of NA (2.3 g over a period of 210 min) resulted in a late rise (from 150 min on) of GH (From 1.1 to 25.9 ng/ml) and an early increase (from 30 min on) of glucagon (from 71.7 to 138.2 pg/ml). When glucose was infused (approximately 60, 120 and 180 g, respectively, over a period of 270 min) during NA-induced FFA depression, the GH rise was reduced and delayed in relation to the amount of glucose infused, but could not be completely abolished (maximal GH concentration during the three NA-plus-glucose infusions: 16.5, 8.0 and 6.1 ng/ml, respectively). The glucagon rise was entirely reversed by the high glucose dose. Insulin did not rise during NA infusion alone. Its secretion in response to glucose infusion was not significantly influenced by FFA depression. Thus, during NA-induced FFA depression the secretion of two lipolytic hormones--GH and glucagon--is stimulated while the secretion of the lipogenetic hormone insulin remains low. Glucose has an inhibitory effect on the GH and glucagon response which, however, is different for each of the hormones.
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PMID:Growth hormone, glucagon, and insulin response to depression of plasma free fatty acids and the effect of glucose infusion. 83 44

Seven men ran at 60% of individual maximal oxygen uptake to exhaustion during beta-adrenergic blockade with propranolol (P), during lipolytic blockade with nicotinic acid (N), or without drugs (C). The total work times (83 +/- 9 (P), 122 +/- 8 (N), 166 +/- 10 (C) min, mean and SE) differed significantly. Epinephrine rose progressively above preexercise levels (0.06 +/- 0.01 ng/ml); at exhaustion concentrations in P experiments (2.15 +/- 0.41) were larger than in N (1.08 +/- 0.31) and C (0.72 +/- 0.28) experiments. Norepinephrine increased consistently while insulin decreased. After an initial decrease glucagon concentrations increased progressively in parallel with declining plasma glucose and were at exhaustion always three times preexercise values. Thus beta-adrenergic blockade did not diminish the glucagon response. Nor was this response increased when alpha-receptor stimulation in P experiments was intensified. Carbohydrate combustion was smaller and NEFA and glycerol concentrations in serum larger during C experiments. Alanine concentrations were never raised at exhaustion. Accordingly, neither stimulation of adrenergic receptors nor NEFA and alanine concentrations are major determinants for the exercise-induced glucagon secretion in man. It is suggested that decreased glucose availability enhances the secretion of glucagon and epinephrine during prolonged exercise.
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PMID:Glucagon and plasma catecholamines during beta-receptor blockade in exercising man. 93 21

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

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


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