Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:034761 (insulin)
 211,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The extracellular space (ECS) of muscle from each ventricle of the heart (RV and LV), the atria, diaphragm, and quadriceps was estimated in the anesthetized rabbit from the distribution volumes of [14C]insulin, [14C]sucrose, [51Cr]EDTA, and C1--. Whole-tissue electrolytes were measured and intracellular electrolytes calculated. The ECS of the tissues varied, increasing in the order quadriceps less than LV less than RV less than atria. The volume of distribution of [14C]inulin was always less than that of either [14C]sucrose or [51Cr]EDTA which agreed closely, whereas that of C1-- was always greater. There was no difference in intracellular K+ in muscle from each of the cardiac chambers, whereas intracellular Na+ and C1-- varied, increasing in the order quadriceps less than LV less than RV less than atria. Intracellular pH, measured with [14C]DMO did not differ in any of the tissues studied. It is concluded that, in vivo, the estimated ECS incardiac muscle is lower than that reported in vitro, that [51Cr]EDTA is a satisfactory ECS marker, and that differences in intracellular Na+ and C1-- but not K+ or pH exist between muscle from the cardiac chambers.
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PMID:ECS, intracellular pH, and electrolytes of cardiac and skeletal muscle. 0 Sep 10

Diabetic ketoacidosis is an acute medical emergency that requires immediate diagnosis and treatment. Diagnosis may be established rapidly by measurement of urinary glucose and ketones, arterial blood pH and blood gases, and serum ketones. Rapid infusion of large volumes of fluids and electrolytes, together with continuous infusion of low doses of insulin, provides effective restoration of fluid and electrolyte balance and correction of metabolic derangements. Hyperosmolar nonketotic coma is characterized by marked hyperglycemia in the absence of ketoacidosis and occurs usually in patients with mild adult-onset diabetes. Symptoms develop more slowly than in diabetic ketoacidosis. Treatment is the same for both conditions. In alcoholic ketoacidosis, hyperketonemia is present without hyperglycemia. The syndrome differs from diabetic ketoacidosis in that blood glucose levels are lower and glycosuria is absent. Treatment consists of intravenous administration of dextrose in water and, if necessary, of sodium bicarbonate. Insulin administration usually is not necessary.
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PMID:Combating diabetic ketoacidosis and other hyperglycemic-ketoacidotic syndromes. 0 17

19F nuclear magnetic resonance spectroscopy has been used to study the effects of salts and denaturants on the structure and aggregation properties of several trifluoroacetyl derivatives of insulin. This technique has been shown to be a powerful tool in the study of specific sites on the protein molecule. Circular dichroic and sedimentation velocity studies were also carried out to aid in the interpretation of the magnetic resonance data. At pH 6.8 Zn2+ had no effect on the 19F magnetic resonance spectrum, however, citrate and acetate ions significantly sharpened the signal from the trifluoroacetyl probe at the N-terminal end (glycine A-1) of the insulin A chain. No alterations were observed in the S20,W value of circular dichroic spectra, suggesting that the probe had gained a considerable degree of motional freedom without changes in aggregation or conformational properties. In the absence of perturbants the trifluoroacetyl group on glycine A-1 showed considerably more motional freedom than on phenylalanine B-1. Guanidine hydrochloride and sodium dodecyl sulfate were used to study the unfolding of several trifluoroacetylinsulin derivatives. The results suggested differential alterations in the environments of the probes located at glycine A-1, phenylalanine B-1, and lysine B-29 in the insulin molecule as the concentration of perturbant was increased.
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PMID:Fluorine nuclear magnetic resonance studies of trifluoroacetylinsulin derivatives. Effects of salts and denaturants. 0 20

13 patients, nine women and four men, aged 22 to 83 years, were treated for diabetic coma or precoma between September 1974 and January 1976. Ten patients were known diabetics and six of them had been treated with insulin. On admission blood sugar was 32.4 +/- 3.3 mmol/l (5.84 +/- 0.6 g/l). The capillary blood pH was 7.15 +/- 0.06 (n = 13). Treatment consisted of continuous insulin infusion (6 IU soluble insulin/hour), physiological saline, potassium substitution and sodium bicarbonate (if the pH was below 7.15). In the first hours of treatment 98 +/- 12IU of insulin, 6.5 +/- 0.5 litres of fluid, 168 +/- 22 mmol of potassium and 237 +/- 55 mmol NaHCO3 were required. During the first 4 hours of the insulin infusion the blood sugar decrease per hour was 3.55 mmol/l (0.64 g/l). Hypokalaemia during treatment occurred in one case, hypoglycaemia was not observed. A preceding treatment with insulin and severe acidosis did not influence therapeutic success. Twelve patients were treated successfully, one patient died 6 hours after admission following mesenteric arterial embolism.
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PMID:[Treatment of diabetic coma and precoma with continuous low-dose insulin infusions (author's transl)]. 1 Oct 87

A membrane fraction enriched in parathyroid hormone (PTH)-sensitive adenylate cyclase and sodium and potassium ion-activated (Na+, K+)-ATPase was prepared from bovine kidney. Tritiated PTH binding to this membrane fraction was dependent on both hormone and membrane protein concentration. Both total and specific binding of the hormone decreased significantly after 5 to 10 min of incubation at 22 degrees. PTH binding was highly specific, being sensitive to inhibition only with active forms of unlabeled hormone (native and 1-34 PTH). Specific binding showed a pH optimum of 7.3 to 7.5. Inhibition of binding of tritiated hormone by unlabeled PTH was also highly effective at pH 6.0, but this apparently specific binding was also inhibited by adrenocorticotropic hormone, insulin, glucagon, and vasopressin. Dissociation of bound hormone was demonstrated, and an apparent dissociation constant of 4.6 X 10(-2) min-1 was obtained. Specific binding was eliminated by pretreatment of the membranes with trypsin. The concentration dependence for inhibition of binding with unlabeled PTH was identical to that for activation of adenylate cyclase in this membrane preparation, and binding was also inhibited by concentrations of calcium in the 0.5 to 2 mM range.
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PMID:Binding of tritiated bovine parathyroid hormone to plasma membranes from bovine kidney cortex. 1 29

Isolated rat lung cell suspensions were prepared by collagenase digestion of the lung stroma. These cells were functionally competent as judged, among other criteria, by their constant rates of oxygen uptake and glucose utilization. An important metabolic feature of these cells is that they display very high glycolytic rates. At least 60% of the glucose utilized was converted to lactate, regardless of the glucose concentration in the medium. The state of reduction of the nicotinamide system, as indicated by the lactate-to-pyruvate ratio, was normal, thus indicating that the high glycolytic fluxes are not related to poor oxygenation of the preparation. Utilization of glucose displayed Michaelis-Menten saturation type kinetics with a Vmax of 331 nmol/10(6) cells per h and an apparent Km of 2.4 mM. These values were not affected by the presence of ouabain (0.1 mM), mannoheptulose (5 mM), or insulin (1 mU/ml), whereas phloridzin produced a drastic inhibition of glucose utilzation showing an apparent Ki of 0.4 mM. The substitution of sodium by K+ or Li+ as the predominant cations in the incubation medium does not alter rates of glucose utilization. Optimal pH for glucose utilization was within the physiological range with a more pronounced inhibitory effect at alkaline pH's. The intracellular concentration glucose was found to be low. This finding, in conjunction with a Q10 (27-37 degrees C) for glucose utilization above 2.0 and the differential effects of D- and L-glucose on production, seems to indicate that a stereospecific glucose transport system exists in lung cells. Several findings point to glucose transport into the lung cells as a probable rate-limiting step for its metabolism:1) the activity of the glycolytic enzymes largely exceeded the observed rate of glucose utilization;2) the decrease in enzyme activity during starvation was not accompanied by a decreased glycolytic flux, suggesting that factors other than enzyme activity, perhaps the supply of fuel, are rate limiting in the overall process of glucose breakdown;3) fructose was able to increase lactate production in the presence of saturating concentrations of glucose. These additive effects of glucose and fructose seem to support the point of view that it is not the glycolytic machinery but the supply of fuel which is rate limiting for glucose utilization by isolated rat lung cells.
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PMID:Metabolic features of isolated rat lung cells. I. Factors controlling glucose utilization. 1 58

In the normal anesthetized dog the combination of insulin, whether of exogenous or endogenous origin, with sodium dichloroacetate provoke a rapid and important reduction of the hyperlactatemia and hyperpyruvicemia induced by the intraduodenal injection of high doses of phenformin. Furthermore this combination prevents the progressive and important lowering of the arterial pH provoked by phenformin.
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PMID:[Actions of sodium dichloroacetate in combination with insulin on hyperlactatemia and hyperpyruvicemia induced in dogs by phenformin]. 2 Jan 98

The beta1- and beta2-components in antidiuresis and sodium retention induced by beta-adrenergic agonists were analysed in ethanol-anesthetized, water-diuretic rats. Intravenous infusions of isoprenaline, salbutamol and carbuterol did not affect insulin clearance but increased plasma renin concentration to the same same extent. Propranolol completely blocked the decreases in urine volume (V) and urinary sodium excretion (UNaV) induced by isoprenaline; practolol (beta1-blocker) inhibited only the decrease in UNaV and butaxamine (beta2-blocker) inhibited only the decrease in V. The ratios of doses of beta-agonists which decreased UNaV and by 50% (ED50 UNaV decrease/ED50 V decrease) were 0.34, 0.68, 1.56 and 2.36 for isoprenaline, tretoquinol, salbutamol and carbuterol, respectively. This increasing order of the ratios coincided with the order reported for the preponderance of the beta2- over beta1-component of these agonists. These results indicate that the decrease in UNaV induced by beta-agonists is related to beta1 stimulation, while the decrease in V is related to beta2 stimulation.
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PMID:Antidiuresis induced by beta1- and beta2-adrenergic agonists in ethanol-anesthetized rats. 2 97

Intact rat epididymal fat-cells were incubated with 32Pi and the intracellular proteins separated by sodium dodecyl sulphate/polyacrylamide-gel electrophoresis. One of the phosphorylated proteins has the same RF value as [14C]biotin-labelled acetyl-CoA carboxylase purified from fat-cells and is specifically precipitated after incubation with antiserum raised against acetyl-CoA carboxylase. No significant changes in the extent of phosphorylation of acetyl-CoA carboxylase were detected after exposure of the cells to insulin.
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PMID:Demonstration of the phosphorylation of acetyl-coenzyme A carboxylase within intact rat epididymal fat-cells. 2 37

Different types of experimental hyperlactatemia and hyperpyruvicemia with or without lowering of blood pH were induced in anesthetized dogs. The initially studied experimental model was the hyperlactatemia and hyperpyruvicemia with lowering of blood pH induced by the intraduodenal administration of high doses of phenformin. Intravenous perfusion of sodium dichloroacetate (150 mg/kg infused during 20 minutes), which acts on the enzymatic complex of pyruvate dehydrogenase, reduced the hyperiactatemia and hyperpyruvicemia with or without acidosis provoked by phenformin injected intraduodenally (30 mg/kg), by intense muscular work, by hypoxia or by continous perfusion or adrenaline. Exogenous or endogenous insulin combined with sodium dichloracetate reduced the hyperlactatemia and hyperpyruvicemia as well as the changes in blood pH provoked by phenformin, more strongly than did sodium dichloroacetate alone. These findings have been confirmed in the conscious dog.
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PMID:[Sodium dichloracetate: its application to the therapeutics of experimental hyperiactatemia (author's transl)]. 2 98


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