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)

A method for tubeless, double-contrast examination of the small bowel is described. Oral contrast medium and capsules which effervesce in the small bowel resulted in double-contrast demonstration of the small bowel in 90 out of 130 patients. Transit through the small bowel was reduced to an average of 78 minutes, due to increased peristalsis resulting from distension by the intralumental gas. For comparison, average transit time in a control group of 83 patients was found to be 126 minutes. The differential diagnosis of stenosing processes and additional information concerning space-occupying lesions was furthered by small bowel hypotonia induced by the intravenous injection of 15 to 45 mg. propantheline bromide (Probanthine) or 1 to 2 mg. glucagon. The method has the following advantages: 1. Improved demonstration of detailed mucosal pattern, 2. Reduced examination time and 3. Simultaneous visualisation of the entire small bowel.
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PMID:[Double-contrast examination of the small bowel without intubation (author's transl)]. 13 39

Transit times were evaluated in 23 obese subjects before and 1,4 and 12 months after biliopancreatic by-pass. A modified version of the method of Hinton et al. was used to determine emptying of the stomach and partial and total transit times. Emptying of the stomach was normal preoperatively. After surgery, it was almost immediate, except in two subjects with stomitis. Both transit times were virtually unchanged. Since the segment between the stomach and the ileocaecal valve is only half as long as in the normal subject, the results show that the by-pass leads to a slowing of transit that concerns the small intestine only, is quickly established, and does not change in the course of time. Evaluation of the altered anatomical and functional situation, and the absence of a correlation between the long-term behaviour of transit times on one hand and of lipid malabsorption and weight loss on the other-hand, suggest that a slower transit time must not be regarded as a compensation mechanism, except insofar as it restricts the degree of malabsorption set up immediately after surgery. Preliminary studies of enterohormonal changes following the by-pass indicate that increased glucagon and decreased motiline values are mainly responsible for slower transit times.
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PMID:[Intestinal transit time in bilio-pancreatic bypass]. 677 38

Eight overnight fasted healthy young volunteers received an intravenous infusion of 0.5 mg furosemide per kg body weight administered in 60 min. This period was preceded and followed by two control periods of one hour each during which physiological saline (o.154 mol/l) was administered at a rate of 1 ml/min. Furosemide markedly increased the diuresis and natriuresis which reached 1260 +/- 198 ml and 138.4 +/- 20.9 mmol per hour respectively. This was associated with a significant three fold increase in urinary total catecholamines excretion. Blood glucose, plasma free fatty acids, insulin and glucagon concentrations did not exhibit any significant change during and after furosemide infusion, compared to pre-infusion values. These results demonstrate that, in normal man, doses of furosemide capable of exerting plasma concentrations. It is concluded that the stimulation of insulin and glucagon secretion observed in vitro with high furosemide concentrations (5 mmol/l) are not observed under usual therapeutic conditions.
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PMID:Furosemide intravenous infusion in normal man: electrolytic, metabolic and hormonal effects. Lack of changes in basal insulin and glucagon plasma levels. 701 22

The transport of human alpha 1-acid glycoprotein from the circulation to the bile has been studied in the rat. Biliary excretion was proportional to the i.v. injected dose, and the percentage excreted remained constant. The amount excreted in the bile (over 4 hr) was inversely related to the rate of hepatic (hepatocyte) uptake and the galactose receptor which is specific for asialo glycoproteins was not involved. Reinjection of the glycoprotein excreted in bile resulted in a similar proportion of the dose being reexcreted, suggesting that a subset of the glycoprotein is not selected for excretion in bile. Transit times from blood to bile for glucagon, insulin, alpha 1-acid glycoprotein, fetuin, albumin, and carcinoembryonic antigen were directly related to their molecular weights. Removal of sialic acid from the asialo glycoproteins did not affect these transit times. Possible mechanisms for the biliary excretion of alpha 1-acid glycoprotein are discussed.
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PMID:The mechanism of biliary excretion of alpha 1-acid glycoprotein in the rat: evidence for a molecular weight-dependent, nonreceptor-mediated pathway. 714 91

Intracellular hydration may play a role in the regulation of protein and nitrogen metabolism. The hepatic removal of nitrogen by urea synthesis has a key regulatory role in nitrogen balance. The purpose of the present study was to establish the acute effects of dehydration on the hepatic kinetics of urea synthesis, quantified by functional hepatic nitrogen clearance (FHNC), in healthy volunteers. Seven healthy men were studied twice in random order. On both study days, a primed continuous infusion of alanine was given. On the day of dehydration an intravenous bolus injection of a loop diuretic (furosemide, 1 mg/kg) was superimposed. FHNC was calculated as the ratio between measured synthesis rates of urea nitrogen and blood alanine concentrations. Furosemide induced a weight loss of 1 kg. During dehydration, FHNC decreased by approx. 25% (41+/-11 to 54+/-10 litres/h; P<0.02). On both occasions individual FHNC and glucagon values were positively correlated (r(2)>0.6). In addition, dehydration more than halved the linear slope of the relationship (P<0.05). The FHNC values were correlated with the urinary excretion of both potassium and sodium (r(2)=0.68, P<0.01 and r(2)=0.62, P<0.02 respectively). Changes in the reactivity of urea synthesis to glucagon (i.e. the ratio between FHNC and glucagon concentration) was negatively correlated with an indirectly estimated change in intracellular water (r(2)=0.79, P<0.05). We conclude that acute moderate dehydration down-regulates both total urea synthesis and its sensitivity to glucagon. The latter was related to estimated intracellular water loss. Dehydration may thus have nitrogen-saving consequences with regard to the hepatic contribution to whole-body nitrogen homoeostasis. The mechanism of this effect and the relationship with sodium and potassium fluxes is not known.
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PMID:Acute effects of moderate dehydration on the hepatic conversion of amino nitrogen into urea nitrogen in healthy men. 1156 69