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Biomedical subjects

M Konagaya

Publications and source records attributed to M Konagaya.

At least 73 records · Page 4Linked to original sources
PubMed1987

Glucocorticoid receptor-mediated induction of glutamine synthetase in skeletal muscle cells in vitro.

We studied the regulation by glucocorticoids of glutamine synthetase in L6 muscle cells in culture. Glutamine synthetase activity was strikingly enhanced by dexamethasone. The dexamethasone-mediated induction of glutamine synthetase activity was blocked by RU38486 [11 beta-(4-dimethylaminophenyl)17 beta-hydroxy-17 alpha-(prop-1-ynyl)estra-4,9-dien-3-one], a glucocorticoid antagonist, indicating the involvement of intracellular glucocorticoid receptors in the induction process. RU38486 alone was without effect. Northern blot analysis revealed that dexamethasone-mediated enhancement of glutamine synthetase activity involves increased levels of glutamine synthetase mRNA. Increased enzyme activity was specific for glucocorticoids; other steroid hormones were essentially without effect. The induction of glutamine synthetase was selective, in that glutaminase activity was not induced by dexamethasone treatment of L6 cells. Thus, glucocorticoids regulate the expression of glutamine synthetase mRNA in cultured muscle cells via interaction with intracellular receptors. Such regulation may be relevant to control of glutamine production by muscle.

Animals↗
PubMed1986

A possible role for endogenous glucocorticoids in orchiectomy-induced atrophy of the rat levator ani muscle: studies with RU 38486, a potent and selective antiglucocorticoid.

We employed RU 38486, a potent and selective antiglucocorticoid, to study a possible role for endogenous glucocorticoids in atrophy of the levator ani muscle secondary to castration of male rats. RU 38486 was shown to block [3H]triamcinolone acetonide binding to cytosol from levator ani muscle. Daily oral administration of RU 38486 to castrated rats partially prevented atrophy of the levator ani muscle, as well as a decrease in RNA concentration. In a control group receiving RU 38486 alone, the levator ani underwent significant (20%) hypertrophy. Administration of exogenous dexamethasone also caused pronounced atrophy of the levator ani muscle. This atrophy was prevented, to a significant degree, by simultaneous oral administration of RU 38486. It is concluded that endogenous glucocorticoids, the actions of which are blocked by RU 38486, may be involved in regulation of the mass of the levator ani muscle in intact rats.

Animals↗
PubMed1986

Glutamate dehydrogenase and its isozyme activity in olivopontocerebellar atrophy.

Evaluation of glutamate dehydrogenase (GDH) in 12 patients with olivopontocerebellar atrophy showed deficiency of the enzyme in the group as well as in each patient. The activity of total GDH was 77.7% of that in controls. We also demonstrated two components of this enzyme differentiated by their thermostabilities. The activity of the heat-labile component was remarkably reduced in patients although that of the heat-stable component showed the same magnitude as in controls. These data suggest that GDH deficiency is mainly caused by its heat-labile component deficiency, which might be related to the pathogenesis of this disease.

Aged↗
PubMed1986

Blockade of glucocorticoid receptor binding and inhibition of dexamethasone-induced muscle atrophy in the rat by RU38486, a potent glucocorticoid antagonist.

Glucocorticoid hormones cause marked muscular atrophy, the mechanism of which is unknown. We employed a potent glucocorticoid antagonist, RU38486 [11 beta-(4-dimethylaminophenyl)17 beta-hydroxy-17 alpha-(prop-1-ynyl)estra-4,9-dien-3-one], to determine whether intracellular glucocorticoid receptors are involved. RU38486 was shown to be an effective blocker of glucocorticoid receptor binding in vivo and in vitro. Furthermore, this compound significantly blocked the loss of body and muscle weight caused by injection of dexamethasone. These data indicate that intracellular glucocorticoid receptors are important in the etiology of steroid myopathy. Studies with glucocorticoid antagonists may lead to the design of specific therapeutic modalities for the treatment of both endogenously and exogenously produced steroid myopathies.

Animals↗
PubMed1986

Regularity in the change of serum creatine kinase level in Duchenne muscular dystrophy. A study with long-term follow-up cases.

Changes in the serum creatine kinase (CK) level according to the disease course were regressed to an exponential function Y = A e-ex in each case of 28 Duchenne muscular dystrophy (DMD) through a long-term follow-up study. The regression to this formula implies that DMD muscle would decay by the leaking of a certain amount of CK into the circulation in proportion to the existing muscle. The diminution coefficient "r" was significantly reduced in puberty as compared with ages around ten. The cases of rapid progression showed a high rate of CK decrement in puberty. The diminution rate of CK is suspected to reflect the difference between the rate of muscle growth and primary muscle decay.

Adolescent↗
PubMed1985

Tuberoinfundibular dopaminergic system and anterior pituitary dopamine receptor in Shy-Drager syndrome.

Tuberoinfundibular dopaminergic system (TIDA) together with anterior pituitary dopamine receptor was evaluated in 9 patients with Shy-Drager syndrome (SDS) through the responses of serum growth hormone (GH) and prolactin (PRL) to dopaminergic stimulation or dopamine receptor inhibition. A variety of abnormal responses of serum GH and/or PRL following the administration of these drugs suggests the TIDA involvement as well as the nigrostriatal system and moreover the different degeneration processes in each dopaminergic system in SDS.

Aged↗
PubMed1985

Evaluation of renal parathyroid hormone receptor function in myotonic dystrophy.

Endocrine abnormalities in myotonic dystrophy (MyD) reflect some of the multi-systemic involvement resulting from this disorder. One of these, abnormal insulin secretion, is considered to be caused by receptor dysfunction. Bone abnormalities, cataract and calcium transport defect suggest the abnormal calcium metabolism in MyD. The calcium metabolism is chiefly regulated by parathyroid hormone (PTH). An interest in the similarity between MyD and pseudohypoparathyroidism, which is a disorder of PTH receptor dysfunction, encouraged the authors to evaluate renal PTH receptor function from the responses of urinary adenosine 3',5'-monophosphate (cAMP) and phosphate excretion after administration of human PTH(1-34). The responses of cAMP were high in 3 cases, low in one case, but normal in the 4 other cases. The phosphaturic responses were elevated in 3 cases, reduced in 3 cases, and normal in 2 other cases. Since these abnormal responses closely mimic those in hypoparathyroidism, there may also be renal PTH receptor dysfunction in some cases of MyD. The results of the present study suggest another peptide hormone receptor defect, similar to insulin, which supports the hypothesis of generalised receptor dysfunction in MyD.

Adult↗
PubMed1984

Studies of circulating parathyroid hormone in man by a homologous amino-terminal specific radioimmunoassay.

A homologous radioimmunoassay specific for amino-terminal portion of human parathyroid hormone(PTH) was developed in order to study the clearance of biologically active species of the hormone in the circulation in man. Characterization of the assay system with synthetic analogues of human PTH (1-34) indicated that the carboxyl-terminal region of human PTH(1-34) is an important recognition site. Plasma amino-terminal PTH levels were less than 0.3 ng/ml in all of 35 normal subjects. The levels were elevated above 0.3 ng/ml in 15 of 24 patients with primary hyperparathyroidism. In 5 patients in whom the levels were determined before and after parathyroidectomy, the elevated levels were all normalized within 60 minutes after the removal of adenomata. The disappearance of exogenous human PTH(1-34) was studied after intravenous administration in 17 patients with hypoparathyroidism. A graphical analysis of the data disclosed two major components of the disappearance curve with estimated half-disappearance time of 3 and 28 minutes respectively, suggesting that multiple mechanisms are involved in the clearance of the peptide from the circulation. These results demonstrate usefulness of homologous radioimmunoassay for human PTH(1-34) in diagnosis and management of hyperparathyroidism, as well as in studying the clearance of amino-terminal portion of PTH which is known to represent biological activity.

Humans↗