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)

Glibenclamide has been shown to stimulate an insulin releasing factor in the duodenum. The possibility that this effect is of importance in its hypoglycaemic action was investigated by studying the effect of galactose on insulin release before and after treatment with glibenclamide; galactose stimulates insulin release when given orally but has no effect when given parenterally; thus its ability to release insulin appears to reside in an action on a gut factor. Measurements of plasma glucose, insulin and glucagon were made on twelve maturity onset diabetic patients following an oral glucose tolerance test and an oral galactose tolerance test before and after one week of treatment with glibenclamide. Glibenclamide significantly reduced the blood glucose levels. Both basal insulin and basal glucagon levels were unchanged. The insulin response to oral glucose was enhanced. Glucagon levels before treatment did not suppression of glucagon levels. Galactose stimulated insulin release but insulin levels before and after treatment were identical. An effect of glibenclamide on gut insulin releasing activity was not demonstrated but the galactose tolerance test provides a useful technique by which to examine the enteroinsular axis.
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PMID:The effect of glibenclamide treatment on the insulin and glucagon responses to oral glucose and galactose in maturity onset diabetics. 11 30

Human hepatic stimulator substance (HSS), an organ-specific and heat-stable factor which differs from insulin, glucagon and EGF, has been partially purified from aborted human fetal livers. It was found to stimulate DNA synthesis of human hepatocytes. AH22 hepatoma cells responded dose-dependently. HSS was also found to enhance the survival of D-GAL intoxicated rats as compared to control (62.5% vs. 26.1%). Our results suggest that human HSS is very similar to that in animals.
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PMID:Effects of human HSS on hepatocyte and hepatoma cell proliferation and D-GAL induced acute liver failure. 133 57

We investigated the effect of several potential carbohydrate secretagogues, amino acids, a ketoacid, and potassium chloride on insulin, glucagon, and somatostatin release from the in vitro perfused Brockmann body of channel catfish (Ictalurus punctatus). Mannose (15 mM) stimulated the release of insulin and somatostatin. Fructose (30 mM) induced only a small and transient release of somatostatin. Galactose (15 mM) was not a secretagogue. Likewise, glyceraldehyde failed to stimulate hormone release. Among the amino acids newly tested, alanine and leucine, and also alpha-ketoisocaproic acid were without effect. A high concentration of potassium (25 mEq/liter) induced a pronounced release of insulin and glucagon and a moderate release of somatostatin. In conclusion, a striking similarity exists between catfish and higher vertebrates in their pancreatic endocrine response to hexoses; on the other hand, the catfish Brockmann body appears to respond only to a few of the common stimuli of pancreatic hormone release in mammals.
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PMID:Secretagogues for pancreatic hormone release in the channel catfish (Ictalurus punctatus). 288 40

1. Adenylate cyclase activity and patterns of insulin release in response to various concentrations of glucose were determined in islets of Langerhans isolated from starving, fed, or glucose-loaded rats. 2. Basal and glucagon-stimulated activities of adenylate cyclase were lower in islets from starved than from fed rats. The minimum glucose concentration required for stimulation of insulin secretion was higher, whereas the maximum secretory response to glucose was lower, in islets from starved than from fed rats. 3. Adenylate cyclase activity in islets of Langerhans obtained from fed rats loaded with glucose by intermittent intravenous or intraperitoneal injections over 5h was significantly higher than that seen in islets from normal fed rats. Islets obtained from glucose-loaded rats required a lower glucose concentration for stimulation of insulin secretion and attained a higher maximal response to glucose stimulation than those derived from fed rats. 4. Incubation in vitro of islets isolated from normal fed rats, for periods of 1 to 24h in the presence of high concentrations of glucose resulted in an activation of adenylate cyclase that occurred progressively from 2 to 7h and which was maintained during 24h of incubation. The increase of adenylate cyclase activity in isolated islets incubated for 4h in the presence of glucose was not prevented by addition of cycloheximide or actinomycin D. Galactose or 2-deoxyglucose was ineffective in increasing adenylate cyclase activity, and pyruvate (20mm) was less effective than glucose. 5. It is suggested that glucose or a glucose metabolite may exert long-term effects on islet cell adenylate cyclase.
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PMID:A possible role of adenylate cyclase in the long-tern dietary regulation of insulin secretion from rat islets of Langerhans. 459 Feb 1

Carbohydrate metabolism was studied in a child with atypical glycogen storage disease and Fanconi syndrome. Massive glucosuria, partial resistance to glucagon and abnormal responses to carbohydrate loads, mainly in the form of major impairment of galactose utilization were found, as reported in previous cases. Increased blood lactate to pyruvate ratios, observed in a few cases of idiopathic Fanconi syndrome, were not present. [1-14C]Galactose oxidation was normal in erythrocytes, but reduced in fresh minced liver tissue, despite normal activities of hepatic galactokinase, uridyltransferase, and UDP-glucose 4-epimerase in homogenates of frozen liver. These data suggest a defect in hepatic galactose metabolism not so far identified.
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PMID:Defective galactose oxidation in a patient with glycogen storage disease and Fanconi syndrome. 657 55

Galactose usually is ingested as lactose, which is composed of equimolar amounts of glucose and galactose. The contribution of galactose to the increase in glucose and insulin levels following ingestion of equimolar amounts of galactose and glucose, or lactose, has not been reported in people with non-insulin-dependent diabetes mellitus (NIDDM). Therefore, we studied the effects of galactose ingestion alone, as well as with glucose either independently or in the form of lactose, in subjects with untreated NIDDM. Eight male subjects with untreated NIDDM ingested 25 g glucose, 25 g galactose with or without 25 g glucose, or 50 g lactose as a breakfast meal in random sequence. They also received 50 g glucose on two occasions as a reference. Water only was given as a control meal. Plasma galactose, glucose, glucagon, alpha-amino nitrogen (AAN), nonesterified fatty acids (NEFA), and serum insulin and C-peptide concentrations were determined over a 5-hour period. The integrated area responses were quantified over the 5-hour period using the water control as a baseline. Following ingestion of 25 g galactose, the maximal increase in plasma galactose concentration was 1 mmol/L. The mean maximal increases in plasma galactose concentration following ingestion of 25 g galactose + 25 g glucose or following 50-g lactose meals were similar and were only 12% of that following ingestion of galactose alone (P < .05). The mean galactose area response over the water control for the 25-g galactose meal was 0.95 +/- 0.31 mmol.h/L.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of glucose, galactose, and lactose ingestion on the plasma glucose and insulin response in persons with non-insulin-dependent diabetes mellitus. 824 70

The binding properties of hepatic aldolase (B) were determined in digitonin-permeabilized rat hepatocytes after the cells had been preincubated with either glycolytic or gluconeogenic substrates. In hepatocytes that had been preincubated in medium containing 5 mM glucose as sole carbohydrate substrate, binding of aldolase to the hepatocyte matrix was maximal at low KCl concentrations (20 mM) or bivalent cation concentrations (1 mM Mg2+) and half-maximal dissociation occurred at 50 mM KCl. Preincubation of hepatocytes (for 10-30 min) with glucose or mannose (10-40 mM), fructose, sorbitol, dihydroxyacetone or glycerol (1-10 mM), caused a leftward shift of the salt dissociation curve (maximum binding at 10 mM KCl; half-maximum dissociation at 35 mM KCl) but did not affect the proportion of bound enzyme at low or high KCl concentrations. Galactose and 2-deoxyglucose had no effect on aldolase binding. Inhibitors of glucokinase (mannoheptulose and glucosamine) suppressed the effects of glucose but not the effects of sorbitol, glycerol or dihydroxyacetone. Glucagon suppressed the effects of glucose, fructose and dihydroxyacetone but not glycerol. Poly(ethylene glycol) (PEG) (2-10%), added to the permeabilization medium, increased aldolase binding and caused a rightward shift in the salt dissociation curve. In the presence of PEG (6-8%), the effects of substrates on aldolase dissociation were shifted to higher salt concentrations (50-100 mM versus 35 mM KCl). The effects of substrates (added to the intact cell) on aldolase binding to the permeabilized cell could be mimicked by addition of the phosphorylated derivatives of these substrates to the permeabilized cell. Of the intermediates tested dihydroxyacetone phosphate and fructose 1,6-bisphosphate were the most effective at dissociating aldolase (A50 values of 20 microM and 40 microM respectively). Other effective intermediates in order of decreasing potency were fructose 1-phosphate, glycerol 3-phosphate, glucose 1,6-bisphosphate/fructose 2,6-bisphosphate. These results show that aldolase B binds to the hepatocyte matrix by a salt-dependent mechanism that is influenced by macromolecular crowding and metabolic intermediates. Maximum binding occurs when hepatocytes are incubated in the absence of glycolytic and gluconeogenic substrates and minimum binding occurs in the presence of substrates that are precursors of either fructose 1,6-bisphosphate or triose phosphates. Since the bound form of aldolase represents a kinetically less active state it is proposed that aldolase binding and dissociation may be a mechanism for buffering the concentrations of metabolic intermediates.
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PMID:Substrate modulation of aldolase B binding in hepatocytes. 861 43

Classical provocative stimuli of GH secretion such as insulin-induced hypoglycaemia, arginine, clonidine, glucagon and levodopa have been widely used in clinical practice for approximately 30 years. On the other hand, in the last 10 years new potent stimuli of GH secretion have been proposed, but an extensive comparison with the classical ones has rarely been performed, at least in adults. In order to compare the GH-releasing activity of old and new provocative stimuli of GH secretion, and to define the normative values of the GH response, in 178 normal adults (95 males, 83 females; age range: 20-50 years, all within +/-15% of their ideal body weight), we studied the GH response to: insulin-induced hypoglycaemia (ITT, 0.1IU/kg i.v.), arginine (ARG, 0.5g/kg i.v.), clonidine (CLO, 300 microg/kg p.o.), glucagon (GLU, 1mg i.m.), pyridostigmine (PD, 120mg p.o.), galanin (GAL, 80pmol/kg per min), GH-releasing hormone (GHRH, 1 microg/kg i.v.), GHRH+ARG, GHRH+PD, hexarelin, a GH-releasing protein (HEX, 2 microg/kg i.v.) and GHRH+HEX (0.25 microg/kg i.v.). The mean (+/-s.e.m.) peak GH response to ITT (21.8+/-2.8, range: 3.0-84.0 microg/l) was similar to those to ARG (18.0+/-1.6, range: 2.9-39.5 microg/l) or GLU (20. 5+/-2.2, range: 10.6-36.9 microg/l) which, in turn, were higher (P<0. 001) than those to CLO (8.2+/-1.6, range: 0.3-21.5 microg/l), PD (9. 6+/-1.1, range: 2.2-33.0 microg/l) and GAL (9.3+/-1.1, range: 3.9-18. 3 microg/l). The GH response to GHRH (19.1+/-1.5, range: 2.7-55.0 microg/l) was similar to those after ITT, ARG or GLU but clearly lower than those after GHRH+ARG (65.9+/-5.5, range: 13.8-171.0 microg/l) and GHRH+PD (50.2+/-4.6, range: 17.7-134.5 microg/l) which, in turn, were similar. The GH response to HEX (55.3+/-5.5, range: 13.9-163.5 microg/l) was similar to those after GHRH+ARG and GHRH+PD but lower (P<0.001) than that after GHRH+HEX (86.0+/-4.3, range: 49. 0-125.0 microg/l) which was the most potent stimulus of GH secretion. In this adult population the third centile limits of peak GH response to various stimuli were the following: ITT: 5.3; ARG: 2.9; CLO: 1.5; GLU: 7.6; PD: 2.2; GAL: 4.0; GHRH: 5.0; GHRH+ARG: 17.8; GHRH+PD: 17.9; HEX: 21.6; GHRH+HEX: 57.1. These results confirm that, among classical provocative tests of GH secretion, ITT followed by ARG and GLU are the most potent ones and possess clear limits of normality. GHRH+ARG or PD and HEX are strong stimuli of GH secretion which, however, is maximally stimulated by a combination of GHRH and a low dose of HEX. It is recommended that each test is used with appropriate cut-off limits.
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PMID:Comparisons among old and new provocative tests of GH secretion in 178 normal adults. 1075 75

Galactose is one of the monosaccharides of importance in human nutrition. It is converted to glucose-1-phosphate in the liver and subsequently stored as glycogen, or is converted to glucose and released into the circulation. The increase in plasma glucose is known to be modest following galactose ingestion. Whether this is due to a small increase in hepatic glucose output, or to a relatively large increase in hepatic glucose output but a concomitant increase in glucose disposal, is not known in humans. Therefore, the rates of glucose appearance (Ra) and disappearance (Rd) were determined over an 8-hour period in normal subjects using an isotope dilution technique. The subjects ingested 50 g galactose or water alone in random order at 8 AM on separate occasions. Plasma glucose, glucagon, lactate, urea nitrogen, total amino acids, and uric acid and serum insulin and triglycerides also were determined. Following galactose ingestion, there was a modest transient increase in peripheral glucose and insulin concentrations. This was associated with a modest increase in the glucose Ra. The calculated amount of glucose appearing in the circulation as a result of galactose ingestion was 9.8 g, while the amount of glucose disappearing over the 8 hours was 9.9 g. Thus, following ingestion of 50 g galactose by overnight-fasted men, approximately 20% appears as additional glucose in the circulation. Data obtained in animals suggest that a large amount of the galactose is stored as glucose in glycogen. Nevertheless, the conversion of galactose to glucose in the liver may have been greater than suggested by the increase in glucose appearance in the circulation due to substitution for other gluconeogenic substrates.
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PMID:Glucose appearance rate after the ingestion of galactose. 1117 81

Using Surface Plasmon Resonance (SPR) we investigated the interaction of seven neuropeptides with different characteristics and beta-amyloid (Abeta42) peptide, with membranes containing gangliosides. A wide range of affinities characterized the bindings (K(D) = 10(-3)- 10(-7) M), following the scheme: for GM1, Abeta42 > DYN > SP = GAL = SOM = BRD > OXY = ENK; for GD1a, Abeta42 = DYN = GAL > SP = SOM = BRD = OXY > ENK and for GT1b, Abeta42 > DYN > SP = GAL > SOM = BRD = OXY > ENK. The ganglioside sugar moiety, specifically the sialic acid, had an important role in the interactions. In general the affinities were higher with polysialo, than with monosialo gangliosides. The sensorgrams describing the interactions of Abeta42 and SP with gangliosides differed from the interactions of the other studied peptides. Ca(2+) promoted changes in peptide-glycolipid interactions.
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PMID:Neuropeptides interact with glycolipid receptors: a surface plasmon resonance study. 1144 40


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