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M Yanase

Publications and source records attributed to M Yanase.

At least 109 records · Page 6Linked to original sources
PubMed1984

The mechanism of decreased Na+-dependent D-glucose transport in brush-border membrane vesicles from rabbit kidneys with experimental Fanconi syndrome.

In our previous paper (Yanase, M. et al. (1983) Biochim. Biophys. Acta 733, 95-101) we reported that the Na+-dependent D-glucose uptake into brush-border membrane vesicles is decreased in rabbits with experimental Fanconi syndrome (induced by anhydro-4-epitetracycline). In the present paper we investigate the mechanism underlying this decrease. D-Glucose is taken up into the osmotically active space in anhydro-4-epitetracycline-treated brush-border membrane vesicles and exhibits the same distribution volume and the same degree of nonspecific binding and trapping as in control brush-border membrane vesicles. The passive permeability properties of control and anhydro-4-epitetracycline-treated brush-border membrane vesicles are shown to be the same as measured by the time-dependence of L-glucose efflux from brush-border membrane vesicles. D-Glucose flux was measured by the equilibrium exchange procedure at constant external and internal Na+ concentrations and zero potential. Kinetic analyses of Na+-dependent D-glucose flux indicate that Vmax in anhydro-4-epitetracycline-treated brush-border membrane vesicles (79.3 +/- 7.6 nmol/min per mg protein) is significantly smaller than in control brush-border membrane vesicles (141.3 +/- 9.9 nmol/min per mg protein), while the Km values in the two cases are not different from each other (22.3 +/- 0.9 and 27.4 +/- 1.8 mM, respectively). These results suggest that Na+-dependent D-glucose carriers per se are affected by anhydro-4-epitetracycline, and that this disorder is an important underlying mechanism in the decreased Na+-dependent D-glucose uptake into anhydro-4-epitetracycline-treated brush-border membrane vesicles.

Animals↗
PubMed1984

Influence of lesions in the limbic-hypothalamic system on metabolic response of acetate to daily repeated heat exposure in rabbit.

The effects of lesions in the basal medial hypothalamus and limbic structure on the acetate metabolic responses to daily repeated heat exposure in the liver of rabbits have been investigated. The results obtained were summarized as follows: (1) THe acetate metabolic responses to the 1st heat exposure (heat exposure on the 1st day) were altered by the lesions in the periventricular arcuate nucleus (ARC), ventromedial hypothalamus (VMH), stria terminalis (ST) and dorsal fornix (FX). (2) The acetate metabolic responses to heat exposure were completely abolished by the ten times repetition of heat exposure in the rabbits with lesions in ARC or VMH. They were similar to sham-operated animals. (3) The acetate metabolic responses to heat exposure remained even after the ten times repetition of heat exposure in the rabbits with lesions in ST and FX indicating the differences from sham-operated animals. (4) From these results, it might be suggested that the basal medial hypothalamus and limbic structure participated in the mechanism of acetate metabolic response to the 1st heat exposure, but only these limbic structure played some roles in the complete disappearance process of acetate metabolic responses to heat exposure by the ten times repetition of heat exposure.

Acetates↗
PubMed1984

New acute peritoneal dialysis technique: wire-guide insertion and long-term indwelling of peritoneal catheter.

This paper presents the application of wire-guide insertion of peritoneal dialysis catheter. 30 patients who required acute peritoneal dialysis were treated using a total of 37 peritoneal catheters with the wire-guide method. The catheters were left in place as long as possible (periods totalling 644 days in all). The complication of insertion was minor bleeding with blood-tinged dialysate that tended to clear spontaneously in a few days. Leakage occurred in 17 indwelling catheters but did not occur on the days of insertion. There were 3 episodes of clinical peritonitis, so the infection rate was 1 episode every 7 patient-months. This technique is safer and simpler, i.e. the incidence of peritonitis is lower in long-term indwelling catheters, and so it will contribute to the wider and earlier utilization of peritoneal dialysis.

Adult↗
PubMed1983

Decreased Na+-gradient-dependent D-glucose transport in brush-border membrane vesicles from rabbits with experimental Fanconi syndrome.

The effect of anhydro-4-epitetracycline on sodium gradient-dependent D-glucose transport of rabbit renal brush-border membrane vesicles was studied. The purity of isolated brush-border membrane vesicles as judged by enzyme activities was not different between normal control and anhydro-4-epitetracycline-administered rabbits. There was no difference in estimate of intravesicular volume, either. When NaCl was used for sodium gradient, the overshoot of D-glucose uptake into brush-border membrane vesicles isolated from anhydro-4-epitetracycline-treated rabbits was significantly smaller than that of normal control rabbits. In the cases of NaSCN or Na2SO4, the former was also smaller than the latter, but not significantly so. To avoid the possible effect of membrane potential on D-glucose uptake, the voltage-clamp method was applied. Even in the voltage-clamped condition, the overshoot of D-glucose uptake into vesicles from anhydro-4-epitetracycline-treated rabbits was decreased compared to that of normal rabbits. In vitro incubation of brush-border membrane vesicles with 20 mM anhydro-4-epitetracycline caused no alteration in sodium gradient-dependent D-glucose uptake. Our results demonstrate that there exists a disorder in sodium gradient-dependent D-glucose uptake of renal brush-border membrane in anhydro-4-epitetracycline-treated rabbits, and suggest that this disorder is one of the underlying mechanisms of experimental Fanconi syndrome.

Animals↗
PubMed1983

Effect of furosemide on mitochondrial electron transport system and oxidative phosphorylation.

The effects of furosemide on the mitochondrial electron transport system and on oxidative phosphorylation were explored. Furosemide above the concentration of 2 X 10(-3) mol/l was found to inhibit state 3 (ADP-dependent) respiration of the rat liver, renal cortex, renal medulla mitochondria. State 4 (resting) respiration was not affected by furosemide. Furosemide above the concentration of 7.5 X 10(-6) mol/l (substrate: glutamate-malate), and above 5 X 10(-6) mol/l (substrate: succinate) inhibited the respiration of rat liver mitochondria released by 3,5-di-tert-butyl-4-hydroxybenzylidenemalononitrile (SF 6847). This fact exactly indicates that furosemide inhibits the electron transport system in mitochondria. Furosemide at the concentration of 4 X 10(-3) mol/l inhibited the activities of NADH cytochrome c reductase and succinate cytochrome c reductase in sonicated mitochondrial subparticles of beef heart by 78.2% and 79.2% of control, respectively.

Animals↗