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Biomedical subjects

M Utsumi

Publications and source records attributed to M Utsumi.

At least 145 records · Page 8Linked to original sources

Effects of thyroxine and cold exposure on hypothalamic TRH levels in rats with various pituitary-thyroid states.

The hypothalamic content and concentration of thyrotropin-releasing hormone (TRH) were determined by radioimmunoassay in normal, thyroidectomized, hypophysectomized and cold-exposed rats with or without thyroxine. In normal animals, the single administration of thyroxine (1,5 and 20 microgram/100 g B.W.) altered neither the content nor the concentration of TRH in the hypothalamus. However, seven days' administration of this hormone resulted in the dose-dependent increase in the hypothalamic TRH levels. In thyroidectomized rats the hypothalamic TRH levels were slightly reduced in spite of the marked increase of plasma TSH levels and decrease of pituitary TSH levels. In the animals given thyroxine (10 microgram/100 g B.W.) for 7 days in addition to thyroidectomy, however, the TRH levels exceeded that in the animals which underwent throidectomy alone. The hypothalamic TRH levels were markedly reduced in hypophysectomized rats. Conversely, in hypophysectomized rats given 7 days' thyroxine (1 and 5 microgram/100 g B.W.), the levels were increased dose-dependently. In cold-exposed rats, the plasma TSH levels roughly doubled, but the TRH levels remained unchanged. These findings strongly suggest that the feedback site of thyroxine extends not only to the pituitary gland but also to the hypothalamus, and that thyroxine has an increasing effect of the hypothalamic TRH level, though the mechanism(s) remain to be clarified.

Acclimatization↗

Physiologic role of somatostatin. Insulin release from rat islets treated by somatostatin antiserum.

In order to clarify the physiologic role of somatostatin in insulin release, rat pancreatic islets treated by somatostatin antiserum were incubated in media containing various concentrations of glucose. Insulin release from antiserum-treated islets was significantly elevated above that from nontreated ones at 3.3 and 8.3 mM glucose, while the former was not different from the latter at 16.7 mM glucose. It is suggested that somatostatin plays an important role in the regulation of insulin release in the physiologic range of glucose concentration.

Animals↗

[Measurement of rat plasma and pituitary TSH levels by radioimmunoassay and its application to the study of TSH secretion with special reference to the effect of thyroidectomy, cold exposure, synthetic TRH and aging (author's transl)].

Radioimmunoassay of rat TSH was established with purified rat TSH for iodination, standard rat TSH and anti-rat TSH supplied by NIAMDD. Iodination of rat TSH was performed with the method of Greenwood et al. This assay was successful in application to determine the plasma and pituitary TSH level in rats. In this assay the minimum detectable level was 10 ng/tube of NIAMD-Rat TSH-RP-1. Neither rat GH, prolactin, LH, nor synthetic ACTH interferred with the binding of rat TSH to anti-rat TSH. The recovery rate of TSH added to rat plasma was 80-114%. Intraassay and interassay coefficients of variation were 3.45-7.83% and 3.14-11.33% respectively. Plasma TSH level was 0.47+/-0.04 mug/ml in intact male adult rats and 0.35+/-0.03 mug/ml in pentobarbital-anesthetized ones. Plasma and pituitary TSH levels after thyroidectomy were investigated every second day during 2 weeks. The former gradually elevated until 2 weeks after operation, while the latter, 290+/-30 mug/mg gland before thyroidectomy, were reduced to 70+/-21 mug/mg gland on the 4th postoperative day, and thereafter restored to a certain degree. The changes of plasma TSH level immunoassayed in thyroidectomized rats paralleled those obtained by the bioassay within their detectable ranges. Cold exposure for 60 minutes at 0+/-1 degrees C resulted in the increasing plasma TSH from 0.35+/-0.05 mug/ml to 0.97+/-0.06 mug/ml. After the cessation of cold exposure, plasma TSH levels were restored to the resting levels within 60 minutes. Intravenous administration of synthetic TRH over the range from 0.5 ng to 500 ng resulted in a rapid plasma TSH increment with peak response between 6 and 12 minutes. Minimum effective dose of TRH on TSH release was 0.5 ng. The effect of aging was examined, revealing that plasma TSH levels were 0.35+/-0.03 mug/ml and 0.74+/-0.07 mug/ml at 7-9 weeks and 120-150 weeks after birth respectively, while pituitary TSH were 292+/-17 mug/mg gland and 66+/-13 mug/mg gland in the corresponding week with age respectively. TRH-induced TSH response in the aged rats was attenuated and delayed.

Aging↗

Diurnal variation of the human urinary TRH excretion measured by radioimmunoassay.

Urine TRH was estimated by the radioimmunoassay which was accomplished according to the method of Bassiri and Utiger. Minimum detectable dose of TRH was 25 pg and recovery of TRH ranged from 72% to 112% in our laboratory. Intraassay coefficients of variation were 5.4% to 14.0% and interassay variations were 10.6% to 15.0%. Of the TRH analogues tested, only two (Ser-His-Pro-NH2, Thr-His-Pro-NH2) had potent reactivity to anti-TRH serum in large dose of 100 ng/tube. Urine samples were kept at -20 degrees C after adjusted to pH 3.0 because the inactivation of TRH in urine was markedly dependent on temperature and pH value. Using this radioimmunoassay, diurnal variation of the urinary TRH excretion at regular intervals in normal subjects was observed. Peak TRH excretion occurred around early morning, while minimum of the excretion was observed around noon. Total urinary TRH excretion of 24 hours was 817-1579 ng (M+/-SE: 1241+/-89 ng) in normal subjects. In patients with chronic renal failure, urinary excretions of TRH was obviously lower than those of normal subjects.

Adolescent↗