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)

Administration of glucagon to rats at 25 degrees C had no effect upon their VO2, while administration of noradrenaline or noradrenaline plus glucagon raised the VO2. At 5 degrees C, noradrenaline had no effect upon the cold-enhanced VO2, while glucagon caused a rise of 13.7%, implying increased glucagon sensitivity at 5 degrees C. The glucagon-induced enhancement of VO2 was abolished by concurrent administration of noradrenaline.
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PMID:Acute cold exposure increases the glucagon sensitivity of thermogenic metabolism in the rat. 394 70

The effects of norepinephrine and glucagon on gluconeogenesis were studied in hemoglobin-free perfused liver from rats kept for 1-20 days at 4 degrees C. When rats were starved for 24 h at 4 degrees C, the plasma glucose level of rats exposed to cold for 5, 10, and 20 days was significantly higher than that of rats for 1 day, but hepatic glycogen decreased to the same level in all groups. In the isolated perfused liver, basal rates of oxygen consumption and glucose production increased slightly through 5 days of cold exposure and returned to control levels after 20 days of cold exposure. The rates of glucose production from lactate, pyruvate, sorbitol, and glycerol increased by 20-30% after 5 days of cold exposure. The stimulation of gluconeogenesis from these substrates by norepinephrine and phenylephrine increased markedly at all time periods from 1 to 20 days in the cold, with a maximum at 5 days. The stimulation of glycogenolysis by norepinephrine was not affected by cold exposure. The response to catecholamines decreased markedly in liver perfused with calcium-free medium and/or with phentolamine. The stimulation of gluconeogenesis by glucagon increased only in rats exposed to cold for 20 days. The results obtained suggest that the stimulation of hepatic gluconeogenesis by cold is due to an alpha-adrenergic response, and the activation occurs beyond the interaction of norepinephrine with its receptor.
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PMID:Effect of norepinephrine on gluconeogenesis in perfused livers of cold-exposed rats. 403 79

1. Experiments measuring the rate of oxygen consumption of unanaesthetized new-born rabbits and the blood flow in brown adipose tissue of anaesthetized new-born rabbits are described.2. The increase in rate of oxygen consumption caused by I.V. infusion of noradrenaline, adrenaline and isoprenaline (2 mug/kg.min for 10 min) was blocked by propranalol (I.V. 1 mg/kg) but the increase caused by cold exposure was not. A larger dose of propranalol (5 mg) blocked the calorigenic response to cold exposure as well.3. Infusion of glucagon (I.V. 4 mug/kg.min for 10 min) caused a large increase in the rate of the rabbit's oxygen consumption and in blood flow through its brown adipose tissue. These responses, which reached a maximum within 10 min from the start of the infusion, were not blocked by propranalol (1 or 5 mg/kg).4. Infusion of corticotrophin (I.V. 1 i.u./kg.min for 10 min) also caused a large increase in the rate of oxygen consumption of new-born rabbits. The response reached a maximum about 20 min from the start of the infusion and it was not blocked by propranalol (5 mg/kg).5. These results support the conclusion that noradrenaline is released at sympathetic endings in brown adipose tissue and that the increase in blood flow caused by noradrenaline is secondary to its metabolic action on the tissue. They also suggest the possibility that glucagon and corticotrophin may act directly on brown adipose tissue and stimulate heat production during cold exposure.
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PMID:The effect of propranalol on the calorigenic response in brown adipose tissue of new-born rabbits to catecholamines, glucagon, corticotrophin and cold exposure. 429 85

A soluble somatostatin binding factor was detected in cell-free extracts from chicken pancreas. For binding measurements Tyr1-somatostatin was radio-labeled with 125I by the lactoperoxidase technique. Specific radioactivity of about 18.5 MBq/nmol was achieved. Maximal total binding is approximately 0.17 (B/T) in the presence of 30 mg/l pancreatic protein. The specific binding is 0.10 and is suppressed by addition of 1 mg/l synthetic cold cyclic somatostatin. The dose-response curve of synthetic cyclic somatostatin is in the range of 0.6-600 nmol/l. Ca2+ and reduced thiol-reagents inhibit the specific binding. Insulin, glucagon and corticotropin show a low, and luliberin and reduced somatostatin a high cross-reactivity. Molecular weight was estimated by gel filtration and the specific binding molecule was eluted at a Kav = 0.2 on an Ultrogel (AcA 54) column. This corresponds to Mr 40 000. Electrophoretic properties of the binding complex and semipurification by polyacrylamide disc gel electrophoresis: relative mobility of the 125I-Tyr-somatostatin binding complex is about 0.6. Relative mobilities of binding-protein fractions are 0.71 and 0.74. Highest relative specific binding was detected in the (100 000 g) cytosol fractions. Binding with cell-free extracts from the splenic lobe area was 4-fold higher than that from other parts of the chicken pancreas.
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PMID:Somatostatin binding factor from chicken pancreas. 611 81

The role of the endocrine pancreas in glucose production (Ra), utilization (Rd), and metabolic clearance (R'd) was investigated during acute exposure to cold in normal normothermic dogs. Two ambient temperatures (TaN = +25 degrees C and TaC = -21 degrees C) were selected. At TaC, metabolic rate and glucose turnover of the shivering dogs were 4.3 and 2.4 times, respectively, higher than in dogs resting at TaN. As compared with the pre-experimental period, somatostatin infusion at TaN induced a 25% (arterial) and 34% (portal) glucagon deficiency, while insulin concentration dropped by 59% (arterial) and 74% (portal). Similar values were obtained at TaC for glucagon (39% arterial and 47% portal) and for insulin (52% arterial and 56% portal). At TaN, these simultaneous hormonal alterations provoked a slight reduction in plasma glucose concentration which levelled down to 4.4 mM. This reduction was due to a decrease in Ra, followed by a parallel decrease in Rd whereas R'd remained unchanged. At TaC, plasma glucose concentration dropped to the same level but quickly rose again during somatostatin infusion. This rise was due to a larger reduction in Rd than in Ra, accompanied by an abrupt fall in R'd. This reduction in R'd appears to be an important mechanism able to restore euglycemia during global pancreatic hormone deficiency in cold exposed dogs.
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PMID:Combined effects of cold and somatostatin on glucose kinetics in dogs. 611 59

In dogs, selective insulin deficiency induced by simultaneous somatostatin and glucagon infusion does not alter the high rate of glucose utilization provoked by acute cold exposure. However, both in resting and in shivering dogs, lowering of plasma insulin decreases plasma glucose metabolic clearance significantly.
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PMID:Independence of circulating insulin levels of the increased glucose turnover in shivering dogs. 611 62

The development of the autonomic nervous system in relation to perinatal metabolism is reviewed with particular attention given to the adipocyte, hepatocyte and the A and B cells of the islets of Langerhans. Adrenergic receptors develop in the B cell independently of normal innervation and by the time of birth, in most species studied, the pancreas, liver and adipose tissue respond appropriately to autonomic signals. Birth is associated with a huge surge in circulating catecholamines which is probably responsible for the early postnatal rise in free fatty acids and glucagon concentrations in plasma. beta-Blocking drugs such as propranolol have an adverse effect on fetal growth and neonatal metabolism, being responsible for hypoglycemia and for impairing the thermogenic response to cold exposure. beta-Mimetic drugs are commonly used to prevent premature labour and may help the fetus in other ways, for example, by improving the placental blood supply and the delivery of nutrients by increasing maternal fat and carbohydrate mobilization.
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PMID:The autonomic nervous system and perinatal metabolism. 611 24

The effect of acute cold exposure on the concentration of glucagon in the blood was investigated in man and in intact and adrenalectomized rats. In man fasted overnight acute cold exposure, which caused a twofold increase in O2-consumption resulted in a rapid rise in plasma glucagon. The levels of insulin and blood glucose remained unaltered, while the concentration of serum free fatty acids and beta-hydroxybutyrate increased. In fasted intact rats acute cold exposure lead to similar effects. A close parallelism between the rise in plasma glucagon and the concentration of hepatic cycloAMP was observed. Adrenalectomy did not impair the cold induced rise in plasma glucagon and hepatic cycloAMP. It is concluded that acute cold exposure caused a rapid rise in the concentration of plasma glucagon leading to an increase in the concentration of hepatic cycloAMP, thus enhancing the rate of hepatic gluconeogenesis and ketogenesis. As these alterations were similar in the absence of glucocorticoids and medulla-derived catecholamines, it is suggested that glucagon may play a role in the metabolic adaptation to acute cold exposure.
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PMID:Rapid rise in plasma glucagon induced by acute cold exposure in man and rat. 625 83

A biologically active gastrin analogue, [125I](Nle11)-HG-13, appears to bind specifically to saturable binding sites on isolated rabbit gastric mucosal cells: Kd = 70 pM at pH 7.4 and at 37 degrees C. Increasing incubation temperature from +4 degrees C to +37 degrees C increased specific binding. Gastrin binding was shown to be reversible and the dissociation rate was enhanced with cold gastrin. The binding sites were saturated with 0.2 fmol of labelled gastrin per 10(6) mucosal cells. Gastrin binding was not inhibited by secretin, glucagon, Met-enkephalin, physalaemin, eledoisin, BPP, VIP, carbachol, histamine, atropine or cimetidine. Gastrin analogues (HG-4, HG-8, (Leu15)-HG-17), CCK-7 and gastrin antagonists (proglumide or benzotript) inhibited [125I](Nle11)-HG-13 specific binding. We concluded that isolated cells from rabbit gastric fundic mucosa contain high-affinity binding sites for a gastrin analogue (Nle11)-HG-13.
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PMID:High-affinity binding sites for gastrin on isolated rabbit gastric mucosal cells. 629 Feb 32

It is concluded that besides NA, some other hormones (adrenaline, glucagon, growth hormone, ACTH, insulin and adrenal steroids) are also thermogenic. While brown adipose tissue is the most important site of heat during NA thermogenesis, some other organs, namely muscles, also contribute to thermogenesis due to various hormones. Hormones seem to potentiate heat production due to their action in target organs. Humoral thermogenesis not only can compensate the heat loss from the body of cold exposed individuals, but it can also prevent obesity under conditions of an high caloric intake. Some substance, on the other hand, induce a hypometabolic effect (rT3, hibernation trigger, antabolone, bombesin). Additionally, absence of gonadal steroids induce hibernation. Thus, humoral substances contribute both to the control of hyper- and hypometabolic states.
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PMID:Humoral control of hyper- and hypometabolic states. 631 84


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