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Biomedical subjects

T Kono

Publications and source records attributed to T Kono.

At least 325 records · Page 18Linked to original sources
PubMed1984

Sedimentation characteristics of subcellular vesicles associated with internalized insulin and those bound with intracellular glucose transport activity.

Comparative studies were made on the sedimentation characteristics of microsomal vesicles associated with internalized [125I]iodoinsulin and those bound with intracellular glucose transport activity. Upon linear sucrose density gradient centrifugation, the internalized hormone formed a peak slightly, but significantly, on the higher density side of the peak of intracellular glucose transport activity. After a long centrifugation, the peak of 125I activity became lower and broader than that of glucose transport activity. Internalized 125I activity was also found in the medium-density microsomal fraction, which had little glucose transport activity. Accumulation of 125I activity in the medium-density fraction and that in the low-density fraction were both completed in approximately 10 min. Under basal conditions, little, if any, insulin binding activity was detectable in either the medium- or low-density microsomal fractions; in contrast, some glucose transport activity was always present in the low-density fraction. These results indicate that the subcellular distribution of internalized insulin and of intracellular glucose transport activity are different, suggesting that the pathways of intracellular processing of the insulin receptor and the glucose transport mechanism are different.

Adipose Tissue↗
PubMed1984

High level of plasma inactive renin in Bartter's syndrome.

In 10 cases of Bartter's syndrome, plasma active and inactive renin (AR and IR) were measured by two different methods. First, plasma renin activity (PRA), and total renin activity (TRA) after activating IR with trypsin, were measured by radioimmunoassay (RIA) of angiotensin I (AI) generated from endogenous substrate. And secondly, plasma active renin concentration (ARC) and total renin concentration (TRC) were measured by RIA of AI generated in the presence of an excess of exogenous substrate. The difference between TRA and PRA, and between TRC and ARC were designated as inactive renin activity (IRA) and inactive renin concentration (IRC), respectively. Small amounts of IRA were found only in 2 cases and no IRA in 8 cases. However, the existence of large amounts of IR in Bartter's syndrome was revealed by the IRC determination. This suggests that the shortage of endogenous renin substrate, consumed by the markedly increased AR, may have interfered with the detection of IRA in Bartter's syndrome, though the IR is markedly increased as well. The molecular weights of AR and IR were determined by Sephadex G-100 gel filtration in 3 cases. Both AR and IR seemed to be smaller than those of normal subjects.

Adolescent↗
PubMed1984

Effects of mazindol on lipid metabolism of human adipose tissue in vitro.

The interaction of mazindol with catecholamine in regulating peripheral lipid metabolism was studied in vitro. Noradrenaline-induced and adrenaline-induced glycerol release was augmented by addition of 50 ng mazindol. On the other hand, isoproterenol-induced glycerol release was suppressed by addition of 50 ng mazindol. Basal and dopamine-induced glycerol release was not altered by addition of 50 ng mazindol. These results suggest that mazindol may interact with alpha 2-adrenergic receptors in adipose tissue.

Adipose Tissue↗
PubMed1983

Prostaglandin stimulation of adenosine 3',5'-monophosphate accumulation in cultured chondrocytes in the presence or absence of parathyroid hormone.

The effect of prostaglandin analogues on the cyclic AMP level in cultured chondrocytes were examined. Prostaglandin E1 at 0.4 to 30 microM, increased the intracellular concentration of cyclic AMP in chondrocytes. Its effect was rapid, being evident within 1 min and reaching a maximum in 10 to 20 min. The maximum level was sustained until 30 min after its addition and then decreased gradually. Prostaglandin D2 and E2 also increased the cyclic AMP level in chondrocytes, but they had less effect than prostaglandin E1. Prostaglandin A1 had no effect on the nucleotide level in chondrocytes, although they markedly increased the level in fibroblasts. The time course of stimulation of cyclic AMP accumulation in chondrocytes by prostaglandin E1, D2 or E2 was quite different from that by parathyroid hormone (PTH): the effect of prostaglandin was slower and more sustained than that of PTH. PTH potentiated the effect of prostaglandin E1, E2, or D2 on the cyclic AMP level in chondrocytes and that the combined effects of prostaglandin and PTH were more than additive. Addition of an inhibitor of cyclic nucleotide phosphodiesterase with prostaglandin, PTH or both produced a synergistic effect on the accumulation of cyclic AMP in the chondrocytes. These findings suggest that prostaglandin E1, E2, and D2 increase the synthesis of cyclic AMP and that the combined effect of the prostaglandins and PTH on the cyclic AMP level in chondrocytes is partly attributed to the synergistic synthesis of cyclic AMP in the cells.

1-Methyl-3-isobutylxanthine↗
PubMed1983

Improvement of ejaculatory incompetence with bromocriptine in a man with prolactin-secreting pituitary tumor.

We report a case of a prolactin-secreting pituitary tumor in a man whose characteristic findings were ejaculatory incompetence and no response of gonadotropin to clomiphene. After treatment with bromocriptine ejaculation was normal, gonadotropin responded slightly to clomiphene and the high level of plasma prolactin returned to normal. A Hardy operation was performed to remove the pituitary tumor. The patient continues to receive 2.5 mg. bromocriptine daily to maintain normal ejaculation.

Adult↗
PubMed1982

Effects of temperature on basal and insulin-stimulated glucose transport activities in fat cells. Further support for the translocation hypothesis of insulin action.

Effects of temperature on glucose transport in fat cells were studied. In this system, the basal (no insulin) glucose transport activity was higher at approximately 25-30 degrees C than at 37 degrees C, as previously reported (Vega, F. V., and Kono, T. (1979) Arch. Biochem. Biophys. 192, 120-127). The stimulatory effect of low temperature (or the insulin-like effect) was reversible and apparently required metabolic energy for both its forward and reverse reactions. By lowering the ATP level with 2,4-dinitrophenol, one could separately determine the insulin-like stimulatory effect of low temperature and its inhibitory effect on the transport process itself. The maximum level of stimulation by low temperature was greater at 10 degrees C than at 25-30 degrees C, but the rate of stimulation was considerably slower at 10 degrees C than at 25-30 degrees C. When cells were exposed to low temperature, the glucose transport activity in the plasma membrane-rich fraction was increased, while that in the Golgi-rich fraction was decreased. The Arrhenius plot of the basal glucose transport activity determined in the presence of dinitrophenol was apparently linear from 10 to 37 degrees C and parallel to that of the plus insulin activity measured either in the presence or absence of dinitrophenyl. Insulin itself slowly stimulated the glucose transport activity at 10 degrees C. These results are consistent with the view that (a) low temperature, like insulin, induces translocation of the glucose transport activity from an intracellular storage site to the plasma membrane, (b) insulin stimulates glucose transport activity without changing its activation energy, and (c) subcellular membranes do not entirely stop their movement at a low temperature, e.g, at 10 degrees C.

2,4-Dinitrophenol↗
PubMed1982

Evidence that translocation of the glucose transport activity is the major mechanism of insulin action on glucose transport in fat cells.

The glucose transport activity associated with the plasma membrane-rich and Golgi-rich fractions of fat cells was determined after they were reconstituted into egg lecithin liposomes. When the two subcellular fractions were isolated under conditions that would minimize their cross-contamination, the transport activity in the plasma membrane-rich fraction was found to be increased 6.3- to 8.6-fold by insulin, which was added to cells before homogenization, and that the activity in the Golgi-rich fraction was reduced approximately to one-half. In this study, the glucose transport activity in the plasma membrane-rich fraction (either in the basal or plus insulin state) was solubilized, reconstituted, and assayed with an overall efficiency of 25-35%. Four agents known to have insulin-like effects on the glucose transport activity in intact fat cells (hydrogen peroxide, sodium vanadate, trypsin, and p-chloromercuriphenyl sulfonate) not only increased the transport activity in the plasma membrane-rich fraction, but also decreased the activity in the Golgi-rich fraction. The effect of hydrogen peroxide, unlike that of insulin, was not abolished when the insulin receptor was modified proteolytically. Upon administration of insulin to fat cells, and subsequent elimination of the hormone, the glucose transport activities associated with the plasma membrane-rich and Golgi-rich fractions were affected almost concomitantly towards opposite directions. It is proposed as a working hypothesis that translocation of the glucose transport system to the plasma membrane from the Golgi-rich fraction is the major, if not the sole, mechanism by which insulin stimulates glucose transport in fat cells.

3-O-Methylglucose↗