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)

To study the effects of glucagon-insulin (G-I) infusion on protein synthesis and DNA synthesis in a condition with partial hepatic ischemia, G-I or saline was infused via portal vein for 40 minutes before and after a period of partial hepatic ischemia or following a period of partial hepatic ischemia. Protein synthesis was measured by 14C-leucine incorporation into proteins in incubated liver slices and DNA synthesis by 3H-thymidine incorporation into DNA. Protein synthesis in the postischemic liver was significantly recovered faster and more completely in G-I treated rats. G-I infusion enhanced the DNA synthesis of postischemic liver significantly, peaking 48 hours after the period of partial hepatic ischemia. However, the dosage of G-I infused in this investigation couldn't increase the hepatic tissue blood flow measured by hydrogen gas clearance method. On the histological examination, mitotic index was significantly higher in G-I treated group than in control. These results suggest that G-I infusion could be beneficial effects on the liver in situation with partial ischemic injury and that G-I infusion could remarkably augment hepatic tissue repair following ischemic damage.
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PMID:[Beneficial effects of glucagon-insulin infusion on hepatic protein synthesis and DNA synthesis in partial hepatic ischemia]. 267 61

Short and middle term effects of Acarbose were studied in volunteers on a standardized, low-fibre, mixed diet for the development of tolerance phenomena with gas exhalations and some peptide hormone levels as main parameters. Both hydrogen and methane were measured quantitatively as diurnal profiles. Acarbose caused an about 20-fold increase of H2 exhalation and had only moderate effects on methane production, indicating the presence of fermentable carbohydrates in the large bowel. Methanogenic individuals exhaled significantly less H2 than did non-methanogenic subjects. Changes in blood glucose, serum insulin, GIP, gastrin, and plasma glucagon, caused by Acarbose, reflected delayed glucose absorption and were plausible within the regulatory framework of carbohydrate assimilation. When the Acarbose regime was maintained for 5 weeks on a controlled diet, abdominal sensations like e.g. meteorism declined remarkably while carbohydrate fermentation remained high and lowered GIP was sustained. Thus functional responses of the gastro-intestinal tract to altered carbohydrate supplies, elicited by Acarbose, were found by 3 independent parameters: anaerobic gas production, peptide hormone levels, and subjective abdominal sensations. The objective parameters seem to remain constant in the longer run, while subjective parameters show long-term adaptation.
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PMID:Effect of Acarbose on the production of hydrogen and methane and on hormonal parameters in young adults under standardized low-fibre mixed diets. 298 18

Postprandial hyperglycemia in diabetic patients can be modified by delaying the digestion and/or absorption of dietary carbohydrates. We have studied an orally active alpha-glucosidase inhibitor, Bay 1099, in normal volunteers to determine whether these inhibitors can decrease postprandial rises in serum glucose without causing gastrointestinal symptoms or significant fecal caloric wastage. Six subjects were given 25, 50, or 100 mg of Bay 1099 or placebo before meals for 1 week, each with a 1-week washout period. Fasting and postprandial concentrations of glucose, insulin, glucagon, enteroglucagon, and gastrointestinal inhibitory peptide (GIP) were measured after the first and last dose of Bay 1099, and the fecal excretions of protein, fat, fiber, and total calories were measured on the last three days of each diet. The passage of unabsorbed carbohydrate into the colon was determined by breath hydrogen analysis three times during each study week. Increasing doses of Bay 1099 were found to decrease the postprandial rise in serum glucose concentration, delay the time to peak insulin concentration, and decrease the output of GIP after the meal. No adaptation was apparent after 1 week of therapy. A dose of inhibitor (50 mg tid), which greatly improves postprandial glucose and hormone output in diabetes, was associated with minimal symptoms and no excess fecal caloric losses. Thus, glucosidase inhibitors such as Bay 1099 may be useful in the management of patients with carbohydrate intolerance.
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PMID:Intestinal and metabolic responses to an alpha-glucosidase inhibitor in normal volunteers. 305 29

Phosphorus is the sixth most abundant element in the body after oxygen, hydrogen, carbon, nitrogen, and calcium. It comprises about 1% of the total body weight of humans. Eighty-five percent of it is stored in the bone in the form of hydroxyapatite crystal; 14% is in the soft tissues in the form of energy-storing bonds with nucleotides (ATP, GTP), nucleic acids in chromosomes and ribosomes, 2,3-DPG in the red blood cells, and phospholipids in the cells' membranes. Less than 1% is in the extracellular fluids. Phosphate balance is maintained by multiple systems. The gut is responsible for the absorption of two thirds of the 4-30 mg/kg/day of phosphate intake. Absorption sites are all along the gut; in humans the most active site is the jejunum. The kidney filters 90% of the plasma phosphate and reabsorbs it in the tubuli. In states of hypophosphatemia the kidney can reabsorb the filtered phosphates very efficiently, reducing the amount excreted in the urine virtually to zero. The healthy kidney can excrete high loads of phosphate and rid the body of phosphate overload. Through the vitamin D-PTH axis the endocrine system regulates the phosphate balance by influencing the kidney, gut, and bone. Other hormones, including thyroid, insulin, glucagon, glucocorticosteroid, and thyrocalcitonin, play a lesser role in regulation of phosphate metabolism. Because of the complex control of phosphate homeostasis, various clinical conditions may lead to hypophosphatemia. These include nutritional repletion, gastrointestinal malabsorption, use of phosphate binders, starvation, diabetes mellitus, and increased urinary losses due to tubular dysfunction. The clinical picture of phosphate depletion is manifested in different organs and is due mainly to the fall in intracellular levels of ATP and decreased availability of oxygen to the tissues, secondary to 2,3-DPG depletion. The various manifestations of phosphate depletion are listed in Table 2. The treatment of hypophosphatemia consists of administering enteral or parenteral phosphate salts. An important aspect of dealing with the potentially serious effects of phosphate depletion is to prevent the depletion from happening in the first place. Hyperphosphatemia can occur in renal failure, hemolysis, tumor lysis syndrome, and rhabdomyolysis. The treatment of hyperphosphatemia usually consists of fluid administration (in the absence of kidney failure). In chronic hyperphosphatemia, phosphate binders such as aluminum and magnesium salts can reduce the phosphate load. The use of these phosphate binders is limited by their potential side effects.
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PMID:Consequences of phosphate imbalance. 306 Jan 61

Loading of glucagon on mongrel dogs was performed and the following results were obtained: The effects of glucagon on hemodynamics were decrease in the vascular resistance and increase in the blood flow in the superior mesenteric artery. Therefore, the blood flow of the portal vein was also increased. In the hepatic artery, glucagon also decreased the vascular resistance, when the blood flow was initially increased and then decreased. This might be attributable to the difference in sensitivity between the vascular resistance by glucagon. While administration of glucagon increased the blood flow of the portal vein, it had less effect on the vascular resistance. Though the blood flow of the hepatic tissues by hydrogen gas clearance method correlated favorably with the hepatic inflow measured with electromagnetic flowmeter, local blood flow in the hepatic tissues was not always constant in the liver and had some difference. Concerning change in local blood flow in the hepatic tissues, in low perfusion area, the blood flow was increased by low concentration of glucagon. This change in distribution of the blood flow was presumed to be caused by the portal flow. After simultaneous loading of glucagon and ICG, glucagon accelerated excretion of ICG. After simultaneous loading of glucagon and ICG on cirrhotic and control patients, accelerated excretion of ICG with time course was observed in control group. On the other hand, slightly accelerated excretion was seen in cirrhotics. It was suggested that simultaneous loading test of glucagon and ICG may be useful as a test for dynamic ability of hepatic circulation which can not be obtained by ICG loading test.
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PMID:[The effect of glucagon on hepatic blood flow and ICG excretion]. 382 16

To determine responses to abomasal protein infusion and ruminal acetate: propionate ratios, four lactating Toggenburg goats fed hourly a 70% roughage and 30% concentrate diet were used in a Latin-square design with a factorial arrangement of treatments. Either acetate or propionate was infused ruminally and casein or saline infused abomasally. Estimated net energy and volume of the infusates were similar for all treatments. To examine the effects of treatments on glucose metabolism, 2-carbon-14 propionate was infused ruminally and 6-hydrogen-3 glucose was infused intravenously for 9 and 5 h, respectively. Although glucose concentration in plasma was higher and propionate turnover greater with propionate treatment, percentage of glucose derived from propionate, amount of propionate coverted to glucose, and glucose turnover remained unchanged. No differences in glucose metabolism due to the abomasal casein infusion were evident. To determine the effects of treatment on insulin, glucagon, growth hormone, and prolactin in plasma, samples were collected at 10-min intervals for 3 h at 0400 and 1600 h. No diurnal variation or consistent peaks were observed for any of the hormones nor were treatment effects on plasma concentrations of insulin, growth hormone, or prolactin evident. Glucagon concentration was higher with casein treatment; however, no relationship existed between glucagon in plasma and glucogenic parameters measured.
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PMID:Glucogenic and hormonal responses to abomasal casein and ruminal volatile fatty acid infusions in lactating goats. 390 Jan 58

Since insulin is known to stimulate intracellular hydrogen peroxide production in rat epididymal fat cells, the effects of exogenous hydrogen peroxide on rates of basal and hormone-stimulated lipolysis were investigated in a perifusion system. H2O2 (60 microM) caused a weak and transient stimulation of basal lipolysis that did not interfere with subsequent activation of lipolysis by hormones. More importantly, lipolysis stimulated submaximally with ritodrine (10(-7) M) or glucagon (10(-9) M) was inhibited by H2O2 in a manner similar to insulin, although slight differences in time course were noted. Ritodrine served as a beta-adrenergic agonist resistant to oxidative destruction by H2O2. The inhibition of lipolysis was reversible upon cessation of perifusion with H2O2. These findings ruled out oxidative destruction of the hormone or cell death as explanations for the antilipolytic effect of H2O2. Like insulin, H2O2 also inhibited 1-methyl-3-isobutylxanthine (4 X 10(-6) M)-stimulated lipolysis, but whereas insulin inhibited lipolysis stimulated by dibutyryl-cAMP (4 X 10(-4) M), H2O2 further enhanced it. These findings add another case to the growing list of insulin effects on adipocytes that can be mimicked by exogenous H2O2, and they hint at a site where the mechanisms of action of the two agents may differ.
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PMID:Effects of hydrogen peroxide on basal and hormone-stimulated lipolysis in perifused rat fat cells in relation to the mechanism of action of insulin. 615 57

Paired indirect immunoenzyme staining based on primary antisera from the same species was performed sequentially without intermediate antibody elution. The first antigen was labelled brown by an immunoperoxidase procedure (either the two-stage indirect method, the unlabelled antibody peroxidase-antiperoxidase method, or the avidin-biotin bridge method using diaminobenzidine (DAB) and hydrogen peroxide as the substrates. The second antigen was labelled blue by applying a two-stage indirect immuno-alkaline phosphatase procedure using naphthol AS phosphate and Fast Blue BB salt as the substrate. In this way, polyclonal mucosal immunocytes were revealed in distinctly contrasting colours when stained for kappa and lambda light chains. Glucagon and somatostatin (D) cells in human pancreatic islets, and gastrin and D cells in human gastric antral glands, were likewise clearly differentiated. Conversely, a mixed colour appeared in some immunocytes after staining for alpha and kappa chains. However, unbalanced colour mixing was sometimes difficult to interpret, and additional experiments demonstrated that unwanted interactions could take place between the two sequences of reagents if the density of the DAB deposits was insufficient. These pitfalls were incompatible with unequivocal double staining in the same cell. Nevertheless, paired staining could be conveniently applied with the described procedures when prior knowledge had established that the antigens in question were located in separate cells.
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PMID:Paired indirect immunoenzyme staining with primary antibodies from the same species. Application of horseradish peroxidase and alkaline phosphatase as sequential labels. 620 74

In a new approach for the determination of polypeptide conformation, experimental data on intramolecular distances between pairs of hydrogen atoms obtained from nuclear Overhauser enhancement studies are used as input for a distance geometry algorithm. The algorithm determines the limits of the conformation space occupied by the polypeptide chain. The experimental data are used in such a way that the real conformation should in all cases be within these limits. Two important features of the method are that the results do not depend critically on the accuracy of the distance measurements by nuclear Overhauser enhancement studies and that internal mobility of the polypeptide conformation is explicitly taken into consideration. The use of this new procedure is illustrated with a structural study of the region 19-27 of glucagon bound to perdeuterated dodecylphosphocholine micelles.
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PMID:Combined use of proton-proton Overhauser enhancements and a distance geometry algorithm for determination of polypeptide conformations. Application to micelle-bound glucagon. 626 Feb 18

Acarbose, an alpha-glucosidase inhibitor, lowers the glycemic excursion following the ingestion of carbohydrates, in particular, sucrose. This was confirmed with increasing doses of acarbose (0, 50, and 100 mg) and the causes investigated. The absorption of the glucose moiety of sucrose was determined from plasma tracer concentrations when overnight-fasted normal subjects received a 100-g oral sucrose load labeled with sucrose [(1-14C]glucose and a simultaneous intravenous infusion of [3-3H]glucose. As the dose of acarbose given with the sucrose load was increased from 0 to 100 mg, the percentage of the load appearing in the peripheral circulation decreased from 90% to 62%. Malabsorption was confirmed by the appearance of breath hydrogen. Simultaneously, absorption time increased from 243 to 411 min. Maximal glycemic excursions were therefore lowered from 64 to 31 mg/dl. The plasma concentrations of gastric inhibitory polypeptide and insulin decreased with the acarbose dose so that the fractional disappearance rate of glucose also decreased. However, the concentrations of glucagon-like immunoreactivity (GLI) rose, confirming the ileal appearance of malabsorbed sucrose.
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PMID:The effects of an alpha-glucoside hydrolase inhibitor on glycemia and the absorption of sucrose in man determined using a tracer method. 636 57


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