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)

Hypoglycemia is known to stimulate human pancreatic polypeptide (hPP) secretion. To explore further the relationship between glucose availability and hPP release, we have examined the effect of tissue glucopenia induced by 2-deoxy-D-glucose (2-DG) on hPP plasma levels in normal subjects. As this glucose analogue activates the autonomic nervous system, we have also studied the influence of prior atropinization upon the hPP response to 2-DG. Moreover, we have tested the effects of iv epinephrine and norepinephrine on plasma hPP concentrations. Circulating glucagon was also measured. After the iv infusion of 2-DG (50 mg/kg), plasma hPP increased steeply from a fasting value of 104 +/- 24 pg/ml (SEM) to a peak of 2175 +/- 639 pg/ml at 45 min (P less than 0.01) and remained significantly elevated throughout the test. In contrast, prior injection of atropine (1 mg iv) lowered basal hPP levels and reduced conspicuously the hPP response to 2-DG. Epinephrine administration (6 micrograms/min for 60 min) did not significantly modify plasma hPP concentrations. However, 2 h after epinephrine withdrawal, circulating hPP showed a brisk elevation coinciding with the decline of glycemia to subbaseline values. During norepinephrine infusion (6 micrograms/min for 60 min), only a minor and transient increase of plasma hPP was found. Plasma glucagon rose significantly after 2-DG infusion, but this response was virtually absent in the atropine experiment. Whereas the well known glucagon tropic activity of epinephrine was evidenced, norepinephrine failed to exert an obvious effect on glucagonemia. Our data demonstrate that 2-DG induces a powerful stimulation of hPP secretion in normal subjects and suggest that this action is mediated in part, if not entirely, by the parasympathetic nervous system. On the other hand, a major role of the sympathoadrenal system in response of hPP to 2-DG or to hypoglycemia does not seem probable. Finally, the hyperglucagonemic effect of 2-DG seems also to be dependent on cholinergic transmission.
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PMID:Stimulation of pancreatic polypeptide and glucagon secretion by 2-deoxy-D-glucose in man: evidence for cholinergic mediation. 40 Jul 18

Little is known on the enteral stimuli for gastro-intestinal hormone release in newborn infants. We have compared the effect of the first feed of human breast milk (5 ml/kg) or 10% dextrose (5 ml/kg) on blood glucose and plasma gastrin, enteroglucagon, Gastric Inhibitory polypeptide (GIP), pancreatic glucagon, and insulin in 21 full-term infants at 4--6 hours of age. The first feed of human milk caused a rise in blood glucose and plasma insulin, gastrin and enteroglucagon, but no change occurred in GIP or pancreatic glucagon. The 10% dextrose feed did not stimulate enteroglucagon release, although similar changes occurred in blood glucose and plasma insulin and gastrin. We conclude that the composition of the feed influences the pattern of gastro-intestinal hormone release during the first hours of life and that the entero-insular responses to feeding differ in the neonate and the adult.
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PMID:The effect of feeds of differing composition on entero-insular hormone secretion in the first hours of life in human neonates. 41 93

An anomeric specificity of the glucose sensors of A cells and B cells of the pancreas has been reported. In this context the present authors investigated, using the canine intestinal loop prepared from the terminal portion of the ileum, how glucagon-like immunoreactive materials (GLI) of the gut would respond to glucose anomers in an attempt to explore a possible anomeric specificity of glucose-stimulated gut GLI secretion. As a result GLI was found to be more readily released into the blood stream after an intestinal alpha-glucose load than following beta-gluocse during a 15-minute observation period. It is thus suggested that gut GLI-secreting cells have glucose sensors similar to those of pancreatic A or B cells which are specific for the alpha-glucose anomer.
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PMID:Anomeric specificity in the response of gut glucagon-like immunoreactive materials to glucose. 44 2

10 mM D-galactosamine enhibited protein synthesis (1 h incubation time) by 67% in isolated mouse liver cells. Counteracting uridylate deficiency induced by D-galactosamine by preventive administration of 20 mM uridine did not decrease the extent of protein synthesis inhibition. 20 mM D-galactose reverted the inhibition of protein synthesis by D-galactosamine. 10(-5) M epinephrine and 10(-7) M glucagon decreased the incorporation of D-galactosamine into glycogen to 38% and 26% of the control value, respectively, after a 35 min incubation and reduced the inhibition of protein synthesis by D-galactosamine effectively. Experimental evidence supports the view that aminoglycogen formed after D-galactosamine treatment is responsible for the inhibition of protein synthesis.
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PMID:Epinephrine and glucagon counteract inhibition of protein synthesis induced by D-galactosamine in isolated mouse hepatocytes. 47 53

An instrument for the control of blood glucose in a closed-loop fashion has been developed. This artificial beta cell consists of 4 subunits: a Glucose Monitor, a Microcomputer, an Insulin Infusion Pump and a Printer. Its internal control algorithm was derived from the modeled dynamics of glucose-induced insulin secretion, and includes the effects of both the proportional and derivative actions of blood glucose concentration, and is expressed as: IIR = Kp . BG + Kd . deltaBG + Kc, where IIR is insulin infusion rate, BG and deltaBG are blood glucose concentration and rate of change in glycemia, respectively. Kp and Kd are individual coefficients and Kc is a constant of basal insulin secretion. The performance of this system was studied with various kinds of glucose challenges on anaesthetized depancreatized dogs. Its notable characteristics were: 1) the insulin infusion rate was such as to maintain physiological insulin levels, and 2) dextrose or glucagon infusions were not required.
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PMID:The development of an artificial beta cell system and its validation in depancreatized dogs: the physiological restoration of blood glucose homeostasis. 48 66

The concentrations of both GH and prolactin in the circulation of the domestic fowl have been determined after various treatments known to affect carbohydrate metabolism. Fasting decreased the level of glucose, stimulated the secretion of GH and inhibited the secretion of prolactin. Administration of insulin significantly depressed the level of GH in the plasma of normal or fasted birds and also in chickens which had received simultaneous injections of glucose or 2-deoxy-D-glucose. No consistent effect of insulin on the secretion of prolactin was observed. Hyperglycaemia subsequent to administration of glucose had no effect on the levels of either GH or prolactin. Glucagon-induced hyperglycaemia suppressed the level of GH in the plasma and stimulated that of prolactin.
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PMID:Influence of fasting, glucose and insulin on the levels of growth hormone and prolactin in the plasma of the domestic fowl (Gallus domesticus). 63 22

Responses of plasma immunoreactive gastric inhibitory polypeptide (IRGIP) to oral triglyceride or galactose were compared in normal and mildly diabetic (non-insulin-dependent) subjects. After triglyceride the responses of IRGIP were similar, but after galactose those of the diabetics were slightly exaggerated. Both stimuli evoked increments of plasma immunoreactive glucagon (IRG) in diabetics but not in normal subjects. Plasma immunoreactive insulin (IRI) did not change. In normal subjects given oral triglyceride or galactose followed by intravenous (I.V.) glucose the early-phase response of plasma IRI was enhanced and glucose tolerance improved. In the diabetics, oral triglyceride did not affect insulin release or glucose tolerance after I.V. glucose; oral galactose elicited a slight increase of insulin release without improving glucose tolerance. In the diabetics the rise of plasma IRG after ingestion of triglyceride or galactose was maintained after I.V. glucose. It is concluded that endogenous GIP is insulinotropic and that there is partial resistance to this action in diabetes. The results were compatible with feedback inhibition of GIP secretion by insulin and with the suggestion that the rise of plasma IRG associated with secretion of GIP in diabetics may be due to the glucagonotropic action of this peptide.
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PMID:Effects of ingestion of triglyceride or galactose on secretion of gastric inhibitory polypeptide and on responses to intravenous glucose in normal and diabetic subjects. 64 Feb 38

Spontaneous fasting hypoglycemia developed in four nondiabetic patients with end-stage renal failure. All were undergoing long-term maintenance hemodialysis and three patients were anephric. Hypoglycemia was generally accompanied by severe metabolic acidosis and, in three patients, lactic acidemia. Abnormalities of hepatic structure and/or function were present in three patients. In one patient, hypoglycemia was refractory to exogenous glucagon, failed to respond to alanine, glycerol, or galactose, and was associated with suppressed plasma insulin and elevated plasma glucagon levels. Fasting hypoglycemia appeared to result from several mechanisms. In at least two patients, fasting hypoglycemia and lactic acidosis resulted from impaired hepatic gluconeogenesis in association with impaired or absent renal glucose production. Additionally, substrate limitation probably contributed to hypoglycemia in several patients.
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PMID:Spontaneous hypoglycemia in chronic renal failure. 68 26

The effects of L-leucine, D-leucine, and L-isoleucine upon the secretion of glucagon and insulin were investigated using the isolated, perfused rat pancreas. All experiments were conducted in the presence of 5.6 mM D-glucose. Ten-minute perfusions of 2, 5, and 10 mM L-leucine induced the release of glucagon and insulin in a dose-related manner. The removal of L-leucine was followed by renewed release of insulin ("off-response") but not of glucagon. The magnitude of the off-response was greater when L-leucine was perfused over longer periods. L-Isoleucine evoked the release of both glucagon and insulin. When L-leucine was administered during perfusion of L-isoleucine, L-leucine-induced release of glucagon was inhibited, that of insulin was augmented, and the insulin off-response prevailed. When the perfusion of L-leucine immediately preceded that of L-isoleucine, L-isoleucine-induced release of glucagon was abolished and that of insulin was augmented. D-Leucine evoked the release of glucagon but not of insulin, and no off-response occurred. When the perfusion of D-leucine followed that of L-leucine, D-leucine-induced glucagon release was inhibited; the insulin off-response to L-leucine was not altered. We reached the following conclusions. 1) Glucagon release induced by L-leucine, D-leucine, or L-isoleucine is likely to be related to the occupancy by these analogous amino acids of transport and/or receptor sites which they share. 2) The insulin off response to L-leucine seems to be evoked by events which take place during the period of administration of L-leucine; these events are not likely to be the release of insulin that occurs during perfusion of L-leucine or the transport of L-leucine into or out of the beta cell. 3) Structurally or chemically similar compounds which are secretagogues both for glucagon and insulin affect the release of these hormones in different ways; these differences are likely to be due to dissimilar mechanisms governing the secretion of the two hormones.
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PMID:L-Leucine-induced secretion of glucagon and insulin, and the "off-response" to L-leucine in vitro. I. Characterization of the dynamics of secretion. 74 40

The respective roles of glucose and insulin in the regulation of glucagon release from the canine stomach were investigated using an isolated blood-perfused preparation. At normal blood glucose and plasma insulin levels, the stomach released small amounts of glucagon. Such basal gastric glucagon release was not modified by hyperglycemia. In contrast, gastric glucagon release was increased by hypoglycemia or 2-deoxy-D-glucose-induced cytoglycopenia. Antibody neutralization of basal circulating concentrations of insulin (10 +/- 1 microU/ml) doubled the stimulation induced by hypoglycemia alone. It is concluded that: 1) suppression of gastric glucagon release is observed with very low concentrations of insulin; 2) basal gastric glucagon release is not further suppressed by hyperglycemia; and 3) that hypoglycemia and cytoglycopenia stimulate gastric glucagon secretion.
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PMID:Glucose and insulin in the regulation of glucagon release from the isolated perfused dog stomach. 74 4


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