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Biomedical subjects

T Kono

Publications and source records attributed to T Kono.

At least 379 records · Page 21Linked to original sources
PubMed1978

Effects of insulin on the uptake of D-galactose by isolated rat epididymal fat cells.

In muscle, insulin stimulates uptake of D-galactose as well as D-glucose and certain other sugar isomers (Kono, T. and Colowick, S.P. (1961) Arch. Biochem. Biophys. 93, 514--519). In fat cells, the hormone also stimulates uptake of D-glucose and certain other monosaccharides. Nonetheless, the hormone does not increase the uptake, as determined by the utilization, of D-galactose by fat cells (Ball, E.G. and Cooper, O. (1960) J. Biol. Chem. 235, 584--588; Kuo, J.F. and Dill, I.K. (1969) Biochim. Biophys. Acta 177, 17--26). As pointed out by Ball and Cooper, this does not necessarily indicate that insulin has no effect on the membrane transport of D-galactose in fat cells. The possible effect of the hormone on transport may not be seen in the utilization data if the intracellular metabolism is considerably slower than the rate of transport and insensitive to insulin.

Adipose Tissue↗
PubMed1978

Inhibition of angiotensin III action by DES-ASP1-,ILEU8-angiotensin II in man.

In 5 normal men intravenous infusion of 600 ng/kg/min of des-asp1-ileu8-angiotensin II (AIIIA) inhibited a rise in blood pressure as well as increase in plasma aldosterone caused by an intravenous infusion of 20 or 100 ng/kg/min of des-asp1-angiotensin II (angiotensin III, AIII). This result and our previous study on simultaneous infusions of 600 ng/kg/min of AIIIA and 20 ng/kg/min of angiotensin II (AII) in the same 5 normal men demonstrate that this dose of AIIIA antagonizes AIII and AII on the adrenal cortex as well as peripheral arterioles and that AIIIA has the same degree of inhibitory effect on the aldosterone-stimulating action of AIII and on that of AII in man.

Adult↗
PubMed1977

Actions of insulin in fat cells. Effects of low temperature, uncouplers of oxidative phosphorylation, and respiratory inhibitors.

When isolated rat epididymal fat cells were incubated with [125I]iodoinsulin for 5 min at 37 degrees, radioactivity accumulated in the plasma membrane fraction (Peak 1) and an unidentified particulate fraction (Peak 2) as reported previously (Kono, T., Robinson, F.W., and Sarver, J.A. (1975) J. Biol. Chem. 250, 7826-7835). This accumulation of radioactivity in Peak 2 (but not that in Peak 1) was greatly impaired when cells were incubated with iodoinsulin in the presence of a variety of metabolic inhibitors that reduce the cellular content of ATP. The reduction in the ATP level coincided with a disappearance of the stimulatory effects of insulin on sugar transport and the hormone-sensitive phosphodiesterase. In contrast, ATP depletion had no significant effects, at least during a 5-to 15-min incubation, on the intracellular water space and on the basal sugar transport and phosphodiesterase activities. When cells once depleted on ATP by treatment with 2,4-dinitrophenol (1 mM; 10 min) were washed and suspended in fresh buffer, the ATP level was recovered almost fully in 10 min. This recovery coincided with the restoration of responsiveness to insulin. When cells were incubated with [125I]iodoinsulin or insulin for 5 min at 15 degrees instead of 37 degrees, a negligible quantity of radioactivity accumulated in Peak 2 and insulin failed to activate sugar transport. In contrast, under the same conditions, radioactivity accumulated in Peak 1 and insulin stimulated phosphodiesterase considerably. These results suggest that ATP, or some other compound metabolically related to ATP, may be necessary for the actions of insulin on sugar transport and phosphodiesterase. ATP, or some other related compound, may also be necessary in the formation of the radioactive Peak 2, although the physiological function and cellular location of this peak are yet to be ascertained.

Acetylglucosaminidase↗
PubMed1977

Biological activity of high dose of des-asp 1-, ileu 8-angiotensin II in man.

The biological activity of high doses of des-asp 1-, ileu 8-angiotensin II (AIIIA) was studied in man. In 5 normal men an intravenous infusion of 600 ng/kg/min of AIIIA for 30 min caused a slight rise in blood pressure, a decrease in plasma renin activity and an increase in plasma aldosterone. This dose inhibited pressor and steroidogenic actions of angiotensin II infused into the same 5 normal men at a rate of 20 ng/kg/min for 30 min. These results are considerably different from our previous report using lower dose (200 ng/kg/min) of AIIIA and indicate that in man AIIIA has both agonist and antagonist activities on the peripheral arterioles as well as on the adrenal cortex.

Aldosterone↗
PubMed1976

Blood pressure fall by angiotensin II antagonist in patients with Bartter's syndrome.

Intravenous infusion of 600 ng/kg/min of 1-sarcosine, 8-isoleucine-angiotensin II, an angiotensin II antagonist, caused a marked blood pressure fall and a decrease in plasma aldosterone in 3 patients with Bartter's syndrome. These results indicate that proximal cause of Bartter's syndrome is an arteriolar hyporesponsiveness to angiotensin II and that this angiotensin II analogue has an antagonist activity on peripheral arterioles as well as adrenal cortex.

Adult↗
PubMed1976

Biological activity of des-Asp1-,Ileu8-angiotensin II (Ileu8-angiotensin III) in man.

Biological activity of ileu8-angiotensin III (AIIIA) was studied in man. In 5 normal men intravenous infusion of 200 ng/kg/min of AIIIA for 30 minutes from 0900 h had no effect on blood pressure (BP) but caused a decrease in plasma renin activity (PRA) and an increase in plasma aldosterone (PA). This dose did not inhibit pressor and steroidogenic actions of angiotensin II (AII) infused into the normal men at a rate of 20 ng/kg/min for 30 minutes. In 3 patients with Bartter's syndrome 260-1,200 ng/kg/ min of AIIIA infusion for 30 minutes from 0900 h had no effect on BP but caused decreases in PRA and PA. These results indicate that in man AIIIA has no pressor action and no antagonistic effect on pressor action of AII but has PRA-lowering and aldosterone-stimulating effects. Antagonistic effect of AIIIA on steroidogenic action of AII was also shown in patients with Bartter's syndrome but not in AII-treated normal men. This may be due to the difference of administered dose of AIIIA.

Aldosterone↗