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Biomedical subjects

N Takasu

Publications and source records attributed to N Takasu.

At least 199 records · Page 11Linked to original sources
PubMed1982

Rifampicin-induced early phase hyperglycemia in humans.

Early phase hyperglycemia, associated with increased rates of insulin and C-peptide secretion after oral administration of 100 g glucose, was observed among patients with pulmonary tuberculosis who were taking rifampicin. This early phase hyperglycemia appeared shortly after rifampicin was started and it disappeared completely a few days after rifampicin was discontinued. No difference in oral glucose tolerance was noted between healthy normal subjects and patients with pulmonary tuberculosis who were not taking any medications. Antituberculous drugs other than rifampicin did not induce early phase hyperglycemia. Because intravenous glucose tolerance was normal in patients treated with rifampicin, it is suggested that rifampicin produces an early phase hyperglycemia possibly by augmenting intestinal absorption of glucose.

Administration, Oral↗
PubMed1982

Pituitary-thyroid feedback regulation in patients with Graves' disease during antithyroid drug therapy.

In an attempt to study the mode of normalization of thyroid function in patients with Graves' disease, a study was made on 140 patients with Graves' disease who were eumetabolic after appropriate therapy with antithyroid drugs for more than 9 months. T3 administration failed to suppress thyroidal radioiodine uptake and serum T4 in patients with TRH-unresponsive TSH secretion. In addition, exogenous TSH failed to elevate serum levels of T4 and T3. In patients with TRH-responsive pituitaries, T3 administration uniformly made serum TSH undetectable but produced various effects (unsuppressible, partially suppressible, and suppressible) on radioiodine uptake and serum T4. The magnitude of suppression of radioiodine uptake paralleled that of serum T4. In patients with unsuppressible or partially suppressible thyroids, exogenous and endogenous TSH were less effective in elevating serum T4 and T3. In patients with suppressible thyroids, T3 administration depressed radioiodine uptake and serum T4; the magnitudes of depression were comparable to those found in normal subjects. Exogenous and endogenous TSH elevated serum T4 and T3 in patients with suppressible thyroids. Here again, the magnitudes of elevation were comparable to those found in the normal subjects. The serum T3 to T4 ratio was high before treatment, but decreased significantly during antithyroid drug therapy. The magnitude of decrease was roughly proportional to the degree of T3 suppressibility.

Feedback↗
PubMed1982

Refractoriness of TSH- and PGE2-stimulated iodine metabolism in cultured porcine thyroid cells, evidence for refractoriness at the level of cAMP action.

In an attempt to study intrinsic regulatory mechanism involved in iodine metabolism, chronic and acute effects of TSH, PGE2 and DBC on iodine uptake, iodide discharge and organic binding of iodine were examined using cultured porcine thyroid cells. Culture in the presence of TSH, PGE2 and DBC for 6 days maintained the ability to thyroid cells to take up iodine and organify it, but culture in the absence of these substances failed to do so. When incubated with NaI in the presence of 1 mM methylmercaptoimidazole (MMI), the cells took up iodide and this accumulated iodide was discharged by TSH, pGE2 and DBC. TSH-, PGE2, and DBC-stimulated iodide discharge was depressed greatly after chronic exposure to TSH, PGE2 or DBC. This refractoriness of TSH-, PGE2- or DBC-stimulated iodide discharge was not specific for each thyroid stimulating substance; previous exposure to TSH, PGE2 or DBC induced refractoriness of TSH-, PGE2- and DBC-stimulated iodide discharge, providing evidence for the existence of refractoriness at the level of cyclic AMP action on iodide discharge. When incubated with NaI in the absence of MMI, the cells took up iodide and organified it. After 30 min incubation with NaI, TSH, PGE2 and DBC were added and they stimulated iodide organification further. This TSH- and PGE2-stimulated iodide organification was also depressed after exposure to TSH or PGE2. These data indicate that, as an intrinsic regulatory mechanism, refractoriness is operating at the level of cAMP action on iodine discharge and organification.

Animals↗
PubMed1979

Effect of gelatin on the cyclic AMP response of primocultured hog thyroid cells to acute thyrotropin stimulation.

The cyclic AMP response of cultured hog thyroid cells to acute thyrotropin stimulation was shown to be under a dual regulatory control by thyrotropin: both positive and negative regulation have been described. When added to the culture medium, gelatin (0.25%) promoted the reorganization of the cells into folicle-like structures, as does thyrotropin. Unlike thyrotropin, gelatin did not induce an increase in intracellular cyclic AMP but enhanced the acute cyclic AMP response to thyrotropin in cells cultured in gelatin-containing medium. When both gelatin and thyrotropin were present, the positive effect of low concentrations of hormone (less than 50 microU/ml) was increased whereas the refractory process observed in the presence of higher concentrations of hormone (greater than 50 microU/ml) was unchanged. These effects of gelatin might be mediated by interaction of the denatured collagen molecules with external proteins of the plasma membrane of thyroid cells.

Animals↗
PubMed1978

Modulation of adenylate cyclase/cyclic AMP response by thyrotropin and prostaglandin E2 in cultured thyroid cells. 1. Negative regulation.

Isolated porcine thyroid cells, cultured in the presence of thyrotropin (greater than or equal to 0.25 mU/ml) or prostaglandin E2 (greater than or equal to 0.1 micron), showed decreased adenosine 3':5'-monophosphate (cyclic AMP) response to further thyrotropin or prostaglandin E2 stimulation, respectively. Kinetics of the refractory process to thyrotropin and prostaglandin E2 are different: (a) maximal refractoriness to prostaglandin E2 was attained after 2--6 h exposure to prostaglandin E2 while refractoriness to thyrotropin was maximal only after 12--24 h; (b) the degree of refractoriness to prostaglandin E2 was much greater than that to thyrotropin. Refractoriness to thyrotropin or prostaglandin E2 is characterized: by specificity for each thyroid stimulator; by dependence upon the dose of thyrotropin or prostaglandin E2 in culture, e.g. induction of high degree of refractoriness with 0.5 mU/ml thyrotropin (or 1 micron prostaglandin E2), which elicits only a small cyclic AMP increase; by time requirement for induction; by partial effect; by changes of maximum activation of cyclic AMP response; by reversibility. This refractoriness of the cyclic AMP response was not induced by dibutyryl adenosine 3':5'-monophosphate. It was not attributed to increased cyclic AMP-phosphodiesterase activity, but to alterations in the receptor-adenylate cyclase system. Prevention of refractoriness to thyrotropin or prostaglandin E2 by incubation of cells in the presence of actinomycin D, puromycin and cycloheximide suggests that new RNA and protein syntheses are required for the development of the refractory state.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1978

Modulation of adenylate cyclase/cyclic AMP response by thyrotropin and prostaglandin E2 in cultured thyroid cells. 2. Positive regulation.

Two different independent processes are operating in cultured thyroid cells to regulate adenylate cyclase/cyclic AMP responsiveness to thyroid stimulators (thyrotropin and prostaglandin E2): firstly, refractoriness or negative regulation [preceding paper], which is specific for each thyroid stimulator, is not mediated by cyclic AMP and is not accompanied by alteration of adenylate cyclase activity; secondly, positive regulation which is characterized by an augmentation of the cyclic AMP response stimulated by thyrotropin and prostaglandin E2. This process is not specific for each thyroid stimulator and is a state of increased susceptibility of cyclic AMP synthesis to stimulation, accompanied by increased activity of the catalytic subunit of adenylate cyclase. Positive regulation is apparently mediated by increased intracellular cyclic AMP levels. It is a time-dependent and dose-dependent process. Very low concentrations (5-50 micronU/ml) of thyrotropin augmented cyclic AMP synthesis stimulated by thyrotropin and prostaglandin E2 whereas higher concentrations (above 0.1 mU/ml) augmented prostaglandin E2 stimulation but induced refractoriness to thyrotropin. Prostaglandin E2 (0.1 to 10 micronM) augmented thyrotropin stimulation and dibutyryl adenosine 3':5'-monophosphate (0.3 to 2 mM) augmented thyrotropin and prostaglandin E2 stimulation. Positive regulation is a slow process which develops within days and increases up to day 5 in culture. Experiments using inhibitors suggested that protein synthesis is required for the full expression of the increase in adenylate cyclase activity induced by the studied thyroid stimulators.

Adenylyl Cyclases↗
PubMed1976

The different modes of action of thyrotropin and prostaglandin E1 on cyclic adenosine 3',5'-monophosphate synthesis in human thyroid, as studied by sequential stimulations.

PGE1 was equally effective in increasing 3H-cyclic AMP in normal and in toxic thyroids, whereas TSH was less effective but over a longer time in the toxic thyroids. Stimulation by a large second dose of TSH could not be elicited after prior stimulation by large doses of TSH. Similar results were obtained with regard to the effect of PGE1. However, stimulation by a large dose of PGE1 was still effective after the slices became refractory to TSH. Similarly, stimulation by a large dose of TSH was still effective after the slices became refractory to PGE1. It is suggested that the site and/or mode of action of TSH is quite different from that of PGE1.

Cyclic AMP↗