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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For the evaluation of a normal or pathological function of gastric mucosa, a reproducible method for the estimation of the biosynthesis of mucus glycoproteins appears to be necessary. Rat gastric mucosal scrapings incorporate in vitro several labeled compounds such as 14C-U-D-glucose, 35SO4, 14C-I-L-fucose and L-G-3H-proline in glycoproteins similar to those synthetized in vivo by native mucosa. The aim of our present work is to describe in detail the procedure we use and to show its reproducibility in 9 separate experiments. Secreted glycoproteins (fraction II) and intracellular glycoproteins (fraction III) obtained during a 4 hours in vitro incubation of rat gastric mucosal scrapings at 37 degrees C in standardized conditions were separately studied. The protein and hexose contents, total incorporated radioactivity and specific radioactivity (cpm/mg protein) were determined in these two fractions. The protein content of fraction II from 2 rat gastric mucosal scrapings incubated in 5 ml was 2 mg +/- 0.4 SEM and its hexose was 38.7 mg per 100 mg protein +/- 3.9. Fraction III contained 6.3 mg protein +/- 1.3 and 15.7 mg hexose per 100 mg protein +/- 3.5. About 27% of the total radioactivity incorporated (from 14C-glucose) was in fraction II (+/- 2.6 SEM) and 73% (+/- 2.6 SEM) in the cell bound fraction III. The distribution of total radioactivity was quite similar to that of total proteins : about 25% proteins were in fraction II and 75% in fraction III with a SEM of about 5 to 10% of the average value. If the biosynthetic activity is expressed as specific radioactivity, i.e. the ratio of incorporated radioactivity to mg proteins, the average for both fraction II and fraction III was about 10,000 cpm/mg protein and the standard error of the mean values are +/- 5.2% of the mean for in vitro secreted mucus glycoproteins (fraction II) and 9.1% in the case of intracellular glycoproteins (fraction III). These values can be considered as a satisfactory index of reproducibility of the method of mucosal scrapings if performed as described above.
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PMID:Quantitative evaluation of the in vitro biosynthesis of gastric mucus glycoproteins. Standardization of the methodology. 37 65

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

The effects of various hexoses upon immunoreactive insulin (IRI) secretion, glucose disposal, and gastric inhibitory polypeptide (GIP) release have been compared in 10 normal nonobese men. Rapid iv infusion (0.5 g/kg in 3 min) of D-mannose resulted in significant ITI release, the peak levels approaching those after D-glucose infusion. D-Galactose, however, was ineffective. The 60-min urine excretions of mannose, galactose, and glucose were 35 +/- 7%, 16 +/- 4%, and 5.5 +/- 0.7% (mean +/- SEM) of the administered dose, respectively. All subjects also received 50 g oral glucose, mannose, galactose, and fructose on different days, each followed by an iv glucose infusion 30 min later. The ingestion of glucose or galactose resulted in a similar increment of GIP (P less than 0.01), followed by a similar increment in the IRI response to iv glucose. Furthermore, the glucose disposal rate increased 2.5-fold compared to that after iv glucose alone (P less than 0.001). However, oral msnnose or oral fructose caused no significant GIP release, yet the IRI response to a subsequent iv glucose load was moderately augmented after oral mannose or oral fructose when compared to iv glucose alone. In addition, there was a similar enhancement of glucose disposal of the iv glucose load after both oral mannose and oral fructose (P less than 0.01). From these studies we conclude that 1) galactose does not elicit IRI secretion per se, yet, like glucose, potentiates GIP and IRI secretion; 2) mannose, despite weak transport across gut or kidney, evokes significant betacytotropic effects; and 3) mannose- and fructose-induced enhancement of glucose disposal might be mediated by a factor(s) other than GIP.
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PMID:Metabolic effects of glucose, mannose, galactose, and fructose in man. 47 51

Experiments were carried out in anaesthetized pregnant guinea-pigs. Following the maternal injection of a bolus containing 14C-hexose and 3H2O, blood was sampled from the fetal umbilical vein during a single circulatory transit. A placental transfer index was calculated from the ratio of the tracers in the fetal whole blood divided by that in maternal plasma. The transfer index for D-glucose, 0.66 +/- 0.03 (SEM), greatly exceeded that for L-glucose, 0.013 +/- 0.004. Elevation of the maternal plasma D-glucose concentration, with unlabelled D-glucose, resulted in saturation of D-glucose transfer with an apparent Km of 1.2 x 10(-2) mol/l mean maternal plasma D-glucose. Phlorizin at maternal plasma concentrations of approximately 10(-3) mol/l inhibited D-glucose transfer by 40%. Phloretin did not affect D-glucose transfer at levels estimated to be 10(-4) mol/l. Specificity studies with substituted D-glucose analogues showed that alpha-methyl-D-glucoside is not transported by a facilitated pathway; 2-deoxy-D-glucose and 3-O-methyl-D-glucose share the D-glucose carrier and D-galactose has a partial affinity for the D-glucose carrier.
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PMID:Glucose transfer across the intact guinea-pig placenta. 55 Nov 17

We have made serial metabolic observations in 18 acute episodes of alcoholic ketoacidosis in ten patients. Data from patients treated with only saline initially were compared to data from patients who received modest amounts of intravenous dextrose (7.0 to 7.5 gm/hr). More rapid improvement in the acidotic state was seen in the latter group (P less than .001). The quicker decline in absolute levels and ratio of beta-hydroxybutyrate to acetoacetate when glucose was given suggests that this treatment induced mitochondrial oxidation of the reduced form of nicotinamide adenine dinucleotide (NADH). Since phosphorus is a critical cofactor necessary for NADH oxidation and the glucose-induced correction of the acidosis was associated with a rapid decline in serum phosphorus from an initial mean of 6.79 +/- .82 mg/100 ml SEM to 0.96 +/- 0.12 mg/100 ml in 24 hours, we propose that glucose enhanced the mitochondrial capacity to oxidize NADH by increasing hepatocyte phosphorus. This effect combined with decline in free fatty acid levels results in reversal of acidosis. Our data suggest that glucose provides the safest, most effective treatment for this disorder; addition of either insulin or bicarbonate is usually unnecessary.
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PMID:Treatment of alcoholic acidosis: the role of dextrose and phosphorus. 61 32

Glycogen metabolism was studied in the isolated perfused liver of the monkey conceptus at 90% of gestation using an in situ recirculating perfusion system. Net uptake of glucose and galactose and the activities of the enzymes, glycogen synthetase and phosphorylase, were studied in response to varied perfusate composition. Synthetase activity was expressed as %I. the percentage of total synthetase activity in the active form. Perfusate glucose concentrations as high as 700 mg/100 ml did not lead to net glucose uptake of to an increase in the baseline %I synthetase (4 +/- 1, mean +/- SEM). In the presence of 300 mg/100 ml glucose, insulin at 10(-7) M in creased %I to 8 +/- 2, and galactose greater than 75 mg/100 ml increased %I to 8 +/- 1. The combination of galactose, glucose, and insulin increased %I to 40 +/- 5. With this latter combination, synthetase activity was proportional to perfusate glucose concentration above 100 mg/100 ml. Phosphorylase activity was diminished by either galactose or insulin, and phosphorylase activity was lowest in the group receiving galactose, glucose, and insulin. Galactose was taken up by all livers, but net glucose uptake was not observed under any condition; net hexose uptake was observed in perfusions with galactose. Glycogen levels did not vary significantly with varied perfusate composition during the 30-min perfusion periods.
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PMID:Glycogen regulation in isolated perfused near term monkey liver. 81 75

After the infusion of fructose, 0.25 g/kg body wt, the mean peak plasma uric acid level was 5.4 +/- 0.7 (SEM) mg/100 ml in six normal children and was not significantly increased compared with that of the mean basal value of 4.1 +/- 0.5 mg/100 ml. The mean blood inorganic phosphate (Pi) levels were significantly less than the mean fasting value after fructose. Blood glucose, lactic acid, and fructose levels were significantly increased after fructose, but serum magnesium levels did not change. In two patients with hereditary fructose intolerance (HFI) the peak blood uric acid levels were 12.1 and 7.6 mg/100 ml, respectively, after fructose. In both patients the blood glucose concentrations decreased 69 and 26 mg/100 ml below the fasting levels after fructose. The serum Pi level decreased 2.3 and 1.2 mg/100 ml below fasting values, decrements greater than the mean decrement in serum Pi of 0.8 +/- 0.2 mg/100 ml which occurred in six normal children. The mean uric acid excretion, expressed as milligrams per mg urinary creatinine, was 0.6 +/- 0.1 (SEM) before fructose in the normal children and increased significantly to 1.0 +/- mg/mg creatinine after fructose. In two patients with HFI the uric acid excretion increased four- to fivefold after fructose administration; the increased uric acid excretion in HFI exceeded that of normal children. In three patients with galactosemia, increases in blood uric acid levels after galactose ingestion were similar to those in normal children after fructose, but less than those in patients with HFI after fructose. The serum Pi levels decreased less in galactosemic patients after galactose administration than in patients with HFI after fructose infusion. These studies support the hypothesis that fructose-induced hyperuricemia results from degradation of adenosine monophosphate. This effect appears to be specific for fructose. The lack of hyperruricemia in galactosemia patients after galactose ingestion may be explained by the observation that galactose is phosphorylated more slowly than fructose.
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PMID:Fructose-induced hyperuricemia: observations in normal children and in patients with hereditary fructose intolerance and galactosemia. 118 40

Human umbilical vein endothelial cells (HUVEC) cultured in high glucose exhibit delayed replication and colchicine-resistant microtubules. Tubulin dysfunction and stabilization, brought about by acetylation of the NH2-terminal residues, loss of the C-terminal tyrosine and binding of microtubular-associated proteins (MAPs) may be involved in the above phenomenon. The effects of L-tyrosine on HUVEC replication in high glucose were tested and the hypothesis that non-enzymatic glycosylation might impair tubulin depolymerization was also checked by growing the cells in the presence of L-glucose, which binds to intracellular proteins but remains metabolically inactive. After 18 days in culture, the number (mean +/- SEM, n = 7) of HUVEC grown in 28.0 mmol/l D-glucose (435.7 +/- 59.1 x 10(3)) was lower than in 5.6 mmol/l D-glucose (818.3 +/- 75.2 x 10(3)), p < 0.0001. The addition of L-tyrosine 1.7 mmol/l corrected such growth inhibition (623.3 +/- 81.7 x 10(3)), p < 0.0001 vs. D-glucose 28.0 mmol/l, but the cells recovered were less numerous than in physiological glucose alone (p = 0.016). The addition of L-tyrosine to D-glucose 5.6 mmol/l (731.0 +/- 63.2 x 10(3)) did not modify the cell number significantly. HUVEC in extra L-glucose (687.4 +/- 72.0 x 10(3)) were less numerous than in 5.6 mmol/l D-glucose, p = 0.028, but more than in D-glucose 28 mmol/l, p < 0.0001, and were not modified by the addition of L-tyrosine (729.4 +/- 67.1 x 10(3)). HUVEC grown in physiologic and high glucose exhibited specific immunofluorescence for acetylated tubulin and MAPs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Delayed replication of human umbilical vein endothelial cells in high glucose is corrected by L-tyrosine. 128 44

1. Dobutamine in 5% (w/v) D-glucose was infused at sequential doses of 2, 5 and 10 micrograms min-1 kg-1, 45 min at each dose, into eight healthy male subjects, and the effects were compared with those produced by infusion of the corresponding volumes of 5% (w/v) D-glucose alone. 2. The energy expenditure increased and was 33% higher than control (P less than 0.001) at 10 micrograms of dobutamine min-1 kg-1. The respiratory exchange ratio decreased from 0.85 (SEM 0.02) before infusion to 0.80 (SEM 0.01) at 10 micrograms of dobutamine min-1 kg-1, but did not alter during the placebo infusion (P less than 0.001). 3. Plasma noradrenaline concentrations were lower during the dobutamine infusion compared with during the infusion of D-glucose alone (P less than 0.025). Plasma dopamine concentrations remained below 0.1 nmol/l throughout both infusions. 4. Compared with during the placebo infusion, the blood glucose concentration decreased (P less than 0.001), the plasma glycerol and free fatty acid concentrations increased by 150 and 225%, respectively (both P less than 0.001), and the plasma potassium concentration decreased from 3.8 (SEM 0.07) to 3.6 (SEM 0.04) mmol/l (P less than 0.01) during dobutamine infusion. The plasma insulin concentration increased at 2 and 5 micrograms of dobutamine min-1 kg-1 (P less than 0.001) with no further rise at 10 micrograms of dobutamine min-1 kg-1. 5. Compared with during the placebo infusion, the systolic and diastolic blood pressures and the heart rate increased during dobutamine infusion (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic effects of dobutamine in normal man. 131 Sep 21

Acute cellular glucopenia after 2-deoxy-D-glucose administration profoundly stimulates hypothalamic-pituitary-adrenocortical and adrenomedullary activity. Whether glucopenia stimulates sympathoneural release of noradrenaline is unclear. We studied 20 healthy subjects who received 2-deoxy-D-glucose (50 mg/kg in 100 ml isotonic saline) or isotonic saline (100 ml) i.v. for 30 min on each of 2 test days. Heart rate and blood pressure were measured with antecubital venous blood obtained via an indwelling catheter for assays of plasma catecholamines (noradrenaline; adrenaline; dihydroxyphenylalanine; dihydroxyphenylglycol; and dihydroxyphenylacetic acid), corticotrophin, cortisol, and glucose. 2-deoxy-D-glucose decreased diastolic blood pressure by 20% (from 69 +/- 2 to 55 +/- 2 mmHg) and increased adrenaline levels by 30-fold [21 +/- 6 (SEM) to 634 +/- 73 pg/ml], corticotrophin by sevenfold (5.1 +/- 1.2 to 35.8 +/- 4.9 pg/ml), glucose and cortisol by two-fold (82 +/- 5 to 163 +/- 9 mg/dl and 15 +/- 2 to 31 +/- 2 micrograms/dl), and noradrenaline by about 30% (224 +/- 15 to 295 +/- 24 pg/ml, p < 0.05), whereas plasma dihydroxyphenylglycol levels decreased (765 +/- 56 to 628 +/- 42 pg/ml). Small decreases in dihydroxyphenylalanine and dihydroxyphenylacetic acid levels after 2-deoxy-D-glucose did not differ from those after saline. Responses of adrenaline levels were positively correlated with those of noradrenaline (r = 0.47, p < 0.05) and glucose (r = 0.45, p = 0.06), but not of corticotrophin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma levels of catecholamines and corticotrophin during acute glucopenia induced by 2-deoxy-D-glucose in normal man. 133 45


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