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Biomedical subjects

S Tarui

Publications and source records attributed to S Tarui.

At least 343 records · Page 19Linked to original sources
PubMed1984

Responses of catecholamines and other counterregulatory hormones to insulin-induced hypoglycemia in totally pancreatectomized patients.

Responses of glucagon, catecholamines, and other counterregulatory hormones to insulin-induced hypoglycemia were evaluated in five totally pancreatectomized patients and six normal subjects. In pancreatectomized patients, plasma glucagon, probably of gastric origin, did not change significantly during hypoglycemia. The responses of epinephrine and norepinephrine were delayed but adequate compared with those in normal subjects. The responses of cortisol and GH were almost as great as those in normal subjects. However, plasma glucose levels did not recover from hypoglycemia normally in these patients. These results suggest that glucagon responses are essential to recover from hypoglycemia and that neither epinephrine nor norepinephrine plays a crucial role in the recovery from acute insulin-induced hypoglycemia in totally pancreatectomized patients.

Adult↗
PubMed1984

Metabolic basis of improved exercise tolerance: muscle phosphorylase deficiency after glucagon administration.

A 26-year-old girl with muscle phosphorylase deficiency had exercise intolerance and experienced an occasional "second wind" phenomenon. Muscle glycogen concentration was about three times the normal level, whereas each glycolytic intermediate below the phosphorylase step was equivalent to only 10% of a normal level. Semi-ischemic forearm exercise tests disclosed no elevation of the venous lactate or pyruvate level, but they showed remarkable increases of serum creatine kinase and ammonia. Glucagon administration markedly augmented exercise tolerance. Forearm exercise after glucagon injection significantly increased venous lactate. Thus, the beneficial effect of glucagon is attributable to blood glucose utilization by muscle.

Adult↗
PubMed1984

Cytochrome P-450-dependent oxidative cleavage of 1-(tetrahydro-2-furanyl)-5-fluorouracil to 5-fluorouracil.

Cytochrome P-450-dependent oxidative cleavage of 1-(tetrahydro-2-furanyl)-5-fluorouracil (FT) was investigated in a reconstituted system containing purified phenobarbital-inducible cytochrome P-450 (P-450(1)) or 3-methylcholanthrene-inducible cytochrome P-450 (P-448(1)). FT was converted into 5-fluorouracil (5-FU) in the reconstituted system, and its rate was 71 pmol 5-FU formed/min/nmol P-4501 and 45 pmol 5-FU/min/nmol P-448(1). Cytochrome P-450, NADPH-cytochrome P-450 reductase and NADPH were required for 5-FU production. Inhibitors of cytochrome P-450 such as carbon monoxide and metyrapone markedly decreased the rate. FT was found to interact with the purified cytochrome P-450, causing a reverse type I spectral change. From these observations, we concluded that the hepatic microsomal cytochrome P-450-dependent mixed function oxidase system participates in the oxidative cleavage of FT.

Animals↗
PubMed1984

Insulin and epidermal growth factor stimulate glycolysis in quiescent 3T3 fibroblasts with no changes in key glycolytic enzyme activities.

In order to study the effect of insulin and epidermal growth factor (EGF) on glycolysis in quiescent 3T3 fibroblasts and their mechanisms of action, lactic acid produced by cells and activities of key glycolytic enzymes in cell extracts were determined. Insulin increased lactic acid production; the maximal stimulation occurred at the concentrations above 250 ng/ml and the half-maximal dose was 50 ng/ml. This effect of insulin appeared as early as one hour, and lactic acid production in the presence of insulin linearly increased up to 4 h. The 24-h pretreatment with insulin exhibited no significant effect on the production by cells afterward incubated either with or without insulin. Lactic acid production decreased as the concentration of phloridzin increased. However, insulin stimulation of the production still remained in the presence of phloridzin. Parahydroxymercuribenzoate reduced production only by the equivalent of the increase due to insulin. EGF also increased lactic acid production; this effect occurred at 1 ng/ml and was maximal at 100 ng/ml. The activities of hexokinase, phosphofructokinase and pyruvate kinase in quiescent cells were not increased by insulin, and the affinities for substrates of these enzymes remained unaltered. These findings suggest that glucose uptake is a rate-limiting step in glycolysis in quiescent 3T3 fibroblasts and that the stimulatory effect of insulin on glycolysis is mediated by enhanced glucose entry.

Animals↗
PubMed1984

Food constituents as a cause of variation of C-peptide excretion in the urine.

Since C-peptide immunoreactivity (CPR) is excreted at a much higher rate than insulin in the urine, the urinary CPR (U-CPR) level could be a good measure of pancreatic B-cell function. In 10 normal subjects and 17 patients with non insulin-dependent diabetes mellitus (NIDDM), the 24-hour U-CPR level was 49.6 +/- 4.5 (mean +/- SE) micrograms, and 59.1 +/- 7.9 micrograms, respectively. When measured repeatedly during 4-37 consecutive days, the mean levels of coefficient of variation (c.v.) of 24-hour U-CPRs in each individual in normal and diabetic patients were 23.4 +/- 3.2%, and 39.1 +/- 1.2%, respectively. Thus, the daily fluctuation of U-CPR was considerably large not only in NIDDM but also in normal healthy subjects. In order to investigate factors responsible for these U-CPR variations, we analyzed the effect of food constituents on U-CPR excretion in this paper. In 8 healthy subjects 5-hour U-CPR excretions were measured after ingesting 5 kinds of isocaloric 300 kcal test meals, i.e. glucose, starch, protein, fat, and mixed meal which consisted of equal kcal of starch, protein and fat. Five hour U-CPR excretion after glucose, starch and protein meal ingestion was 9.5 +/- 1.3 micrograms, 13.7 +/- 1.9 micrograms, and 7.4 +/- 0.9 micrograms, respectively. Fat meal induced no increase in U-CPR excretion. After the mixed meal ingestion, 5-hour U-CPR was 8.2 +/- 0.6 micrograms, which was approximately the mathematical average for the U-CPR after 3 meals. We conclude that the cause of variations in the U-CPR excretion may be ascribed not only to the ingested total calories, but also to the nutritional components of the diet. Therefore, care must be taken in reading a daily U-CPR measurement in assessing pancreatic B cell function.

Adult↗
PubMed1984

Presence of adrenocorticotropin-potentiating factors in porcine thyroid glands.

An extract of porcine thyroid gland in 0.1 N acetic acid exerted dose-dependent potentiation of ACTH-induced corticosterone production in isolated rat adrenal cells. The extract by itself manifested no steroidogenic activity. Upon gel-filtration of the extract, potentiating activities were demonstrated in three main peaks with molecular weights of about 10,000, 5,000 and 2,000. These findings indicate the presence of heterogeneous forms of ACTH-potentiating factors in the thyroid. Significant enhancement of ACTH-induced steroidogenesis was readily apparent with three gel-filtration fractions at a lower concentration of ACTH (4.75 pM). At this concentration, dose-dependent potentiation was observed with these three fractions. Enhanced corticosterone production responses by cells preincubated with the thyroid extract were observed and the results indicated the existence of potentiating mechanisms other than inhibition of ACTH proteolysis. The lack of T4, T3 and thyroglobulin in this activity suggests that the activity resides in other constituents of the thyroid.

Adrenal Glands↗
PubMed1984

Sensitive non-radioisotopic method for measuring lipoprotein lipase and hepatic triglyceride lipase in post-heparin plasma.

In this method for measuring lipoprotein lipase (LPL) and hepatic triglyceride lipase (H-TGL) in post-heparin plasma, we determine the released free fatty acids enzymically. After release, they are extracted by Dole 's method (J. Biol. Chem. 235: 2595-2599, 1960), solubilized with Triton X-100, then measured with an enzymic kit (NEFA Kit-K; Nippon Shoji Kaisha Ltd.) after residual turbidity is removed by centrifugation with chloroform. A 5-microL sample of post-heparin plasma suffices to measure the activity of LPL and H-TGL; thus the method is as sensitive as the radioisotopic method. Selective assay of LPL and H-TGL, by adding sodium dodecyl sulfate to inactivate H-TGL or NaCl to inactivate LPL, is also feasible. The mean activities +/- SD of LPL and H-TGL in plasma of normal healthy men were respectively 9.4 +/- 2.3 mumol/h per milliliter (157 +/- 38 U/L) and 20.1 +/- 10.4 (335 +/- 173 U) mumol/h per milliliter (U/L).

Adult↗
PubMed1983

Hepatic microsomal cytochrome p-450-dependent N-demethylation of methylguanidine.

Cytochrome P-450-dependent N-demethylation of methylguanidine, a uremia toxin, was investigated. Methylguanidine was stoichiometrically converted into equal amounts of guanidine and formaldehyde by aerobic incubation with phenobarbital-induced microsomes and NADPH. The guanidine formation in the incubation mixture followed Michaelis-Menten kinetics and required the presence of molecular oxygen and NADPH. Methimazole, a non-formaldehyde-producing substrate specific for FAD-containing monooxygenase, did not inhibit significantly formaldehyde formation, suggesting that microsomal FAD-containing monooxygenase does not play a significant role in N-demethylation of methylguanidine. The direct involvement of cytochrome P-450 in the N-demethylation is supported by the observations that addition of methylguanidine to purified cytochrome P-450 preparation caused a type I spectral change and that inhibitors of cytochrome P-450, such as carbon monoxide and metyrapone, markedly decreased the rate of demethylation. Neither superoxide anion nor hydrogen peroxide was directly involved in the demethylation reaction. In addition, guanidine formation was observed in the reconstituted system containing purified cytochrome P-450. Thus, these findings indicate that the hepatic microsomal mixed function oxidase system catalyzes N-demethylation of methylguanidine to guanidine.

Animals↗
PubMed1983

Forskolin-induced cyclic AMP production and gastric acid secretion in dispersed rabbit parietal cells: novel evidence for a major role of cyclic AMP in acid release.

Forskolin, a unique diterpine which is a direct activator of cyclic AMP-generating systems, stimulated both cyclic AMP and acid production in dispersed rabbit parietal cells. This agent was also capable of augmenting the action of histamine on both cyclic AMP and acid production at a low concentration. These findings provided novel evidence for a major role of cyclic AMP in gastric acid secretion.

Animals↗
PubMed1983

Trophic effect of iron-bound transferrin on acetylcholine receptors in rat skeletal muscle in vivo.

Trophic effect of iron-bound transferrin (FeTf) on the total content of acetylcholine receptors (AChRs) and the specific activity of AChRs in innervated and denervated skeletal muscle was investigated in vivo. The right ischiadic nerves of 15 rats weighing 160 g were transected. FeTf (1.2 mg/ml) was injected daily into bilateral crural muscles of rats for the following 11 days. Control groups received injections of saline or no treatment. FeTf significantly increased the total content of AChRs and the specific activity of AChRs in innervated and denervated muscle compared with control groups (P less than 0.001). This result shows that intramuscular injections of FeTf may be useful for the treatment of disorders of neuromuscular transmission.

Animals↗
PubMed1983

Glucose dependent stimulation by prostaglandin D2 of glucagon and insulin in perfused rat pancreas.

Effects of prostaglandin D2 on pancreatic islet function in perfused rat pancreas were examined in comparison with those of prostaglandin E2, which has hitherto been suggested to be a modifier of pancreatic hormone release. In the presence of 2.8 mM glucose, only glucagon release was strongly stimulated by 14 microM of prostaglandin D2, while release of both glucagon and insulin was augmented by 14 microM of prostaglandin E2. When the glucose concentration was elevated to 11.2 mM, insulin release was accelerated by 14 microM of prostaglandin D2 but there was no effect upon glucagon release. Again, release of both glucagon and insulin was augmented by 14 microM of prostaglandin E2 in the presence of 11.2 mM of glucose. The regulation of glucagon and insulin release through prostaglandin D2 is apparently adapted to glycemic changes, and may be a physiological modulator of pancreatic islet function.

Animals↗