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Biomedical subjects

H Fukazawa

Publications and source records attributed to H Fukazawa.

At least 163 records · Page 9Linked to original sources
PubMed1983

Monodeiodination of thyroxine to 3, 5, 3'-triiodothyronine and to 3, 3', 5'-triiodothyronine in isolated dog renal cortical tubuli.

Monodeiodination of T4 to T3 and rT3 in the intact cells of dog renal tubuli and glomeruli was investigated. The tubuli and glomeruli were obtained by a sieve method. T4 (2 micrograms/ml) was incubated in Tris-HCl buffer, pH 7.5, with renal cells (180 micrograms protein/ml) and 5 mM DTT for 1 h at 37 degrees C and the T3 and rT3 generated during incubation were measured by specific radioimmunoassays. In order of decreasing activity, dog renal cortical tubuli, cortical homogenate, glomeruli and medullary tubuli were capable of converting T4 to T3. Net rT3 production from T4 in cortical tubuli was also greater than that in cortical homogenate. The conversion of T4 to T3 and also to rT3 in cortical tubuli was enzymatic in nature, since the reactions showed dependence on time and protein concentration; instability to heating; temperature and pH optimum. The production of T3 and rT3 from T4 was maximum at pH 6.5 and at pH 9.5, respectively, indicating that two different enzymic systems, a 5- and a 5'-monodeiodinase, might be involved in the deiodination of the tyrosyl and the phenolic ring of T4 in dog kidney.

Animals↗
PubMed1983

Recovery of thyroid function with a decreased titre of antimicrosomal antibody in a hypothyroid man with Hashimoto's thyroiditis.

A 36 year old man with a diffuse goitre, signs of mild hypothyroidism, strikingly low levels of T4 (0.9 micrograms/dl) and T3 (24 ng/dl), elevated TSH (140 microU/ml) and elevated microsomal haemagglutination antibody (MCHA, 1:409 600), subsequently became non-goitrous and euthyroid with a decreased titre of antimicrosomal antibody without any medication. At the time of surgical biopsy, serum levels of T4 and T3 had risen to the normal range (4.6 micrograms/dl and 73 ng/dl, respectively), serum TSH had decreased to 30 microU/ml and the titre of MCHA to 1:25 600. Thyroid specimens showed Hashimoto's thyroiditis. The activity of thyroid peroxidase (TPO) was normal. The latest examination, 1 year and 3 months after initial evaluation, showed that the patient remained euthyroid with no goitre, that serum thyroid hormones were within the normal range (T4 7.7 micrograms/dl and T3 97 ng/dl), and that TSH was not detectable. The titre of MCHA decreased strikingly to 1:400.

Adult↗
PubMed1983

Monodeiodination of thyroxine to 3,3',5'-triiodothyronine in the human placenta.

We studied the characteristics of monodeiodination of thyroxine to T3 and reverse T3 in the human placenta which was obtained at normal delivery. The placentas were homogenized in cold sucrose Tris-HCl buffer, pH 7.5. The microsomal fraction was incubated at 37 degrees C in the air for 1 hr with 2 micrograms of T4 in the presence of 0.05 M DTT. The T3 and reverse T3 generated in the reaction mixture were extracted into cold ethanol and measured by RIA. Among the usual subcellular fractions of the placental homogenate, microsomes were most potent in deiodinating T4 to reverse T3, 17.9 ng/mg protein/micrograms T4/60 min. In microsome, production of reverse T3 from T4 was dependent upon protein concentration, incubation temperature, incubation time, pH and T4 concentration, and unstable to prior heating of the microsomal fraction. The production of T3 from T4 was negligible in the present system. Degradation of T3 in the human placenta was rapid. Although addition of anti-T3 antibody to the reaction mixture suppressed the degradation of T3, it had no effect on the net production of T3, suggesting that the obtained net T3 production rate had not been influenced by its degradation. Degradation of reverse T3 was negligible. These results indicate that the human placenta actively deiodinates T4 to reverse T3 enzymatically. This enzyme system might have some influence on the transplacental passage of thyroid hormone from the mother to the fetus.

Dithiothreitol↗
PubMed1983

The features of causes of death in Japanese diabetics during the period 1971-1980.

The principal causes of death among 9,737 diabetics who died in 280 hospitals all over Japan during the period 1971-1980 have been analyzed retrospectively in this study. The main cause of death in Japanese diabetics was vascular complications. The mortality from vascular complications was 41.5%, 37.9% for males and 46.8% for females, increasing with the duration of diabetes and with age. The most interesting findings were of cardiovascular disease which was the cause of death in 12.3% of the subjects in our study as compared to 54.6% of the Joslin Clinic patients (1971). However, our incidence rate was almost twice that reported in Japan in 1967 by Goto (Japan). In contrast, cerebrovascular disease and nephropathy are much more common in Japanese than in American diabetics. Recently cancer has become more common in Japanese diabetics and 25.3% of the deaths have been assigned to it. In contrast, diabetic coma due to hyperglycemia accounted for only 4.1% of deaths. The average life span of Japanese diabetics is still over 10 years shorter than that of non-diabetics.

Adult↗
PubMed1982

[Renal handling of 3,5,3'-triiodothyronine (T3) in the dog studied by stopflow analysis].

In order to investigate the renal handling of 3,5,3'-triiodothyronine (T3), we studied the clearance of T3 (CT3) in dogs and the site of tubular secretion and reabsorption of T3 in dog kidney using the stopflow technique (Malvin et al.). Four female dogs, weighing between 12.2 and 17.8 kg, were used for CT3 measurement. Fourteen anesthetized dogs, weighing between 7.8 and 17.5 kg, were used for the stopflow study. After the catheter was inserted into the left ureter, 15% mannitol solution and isotonic saline containing both 0.2% PSP and 0.5% creatinine or 0.1% inulin, were infused and then 10-30 micrograms/kg of T3 or 100 micrograms/kg of T4 was injected as a bolus. When the urine flow reached a stable state of at least 5 ml/min about one-hr after T3 or T4 injection, the ureteral catheter was clamped shut for 10 min. After the release of the clamp, 20 fractions of urine, 1 ml each, were collected sequentially. The changes in pH and PSP concentrations were used as indices of urine from the distal and proximal tubules, respectively. Urinary T3 was determined by RIA. CT3 was obtained by calculating the ratio of the 24-hr urinary T3 excretion to the serum free T3 concentration. CT3, 51.9 +/- 12.3 ml/min, was greater than the clearance of creatinine (Ccr), 23.8 +/- 4.7 ml/min, suggesting that T3 is secreted at the tubules in dogs. Almost immediately after the release of the clamped ureter, the concentration of urinary T3, corrected with excreted urinary creatinine or inulin, was increased, reaching the maximum value at No. 2 or 3 fraction. This maximum urinary T3 value was followed by decreased concentrations of urinary T3, reaching the minimum around No. 13--15 fraction. The fraction with the highest urinary T3 concentration was close to the one with the lowest pH, and the fraction with the lowest urinary T3 concentration was close to the one with the highest PSP concentration. These data suggest that T3 might be reabsorbed or metabolized at the level of the proximal tubules and secreted into the urine at the level of the distal tubules.

Absorption↗
PubMed1982

[Monodeiodination of thyroxine to 3,3',5'-triiodothyronine in the human placenta].

We investigated the characteristics of the monodeiodination of thyroxine to T3 and rT3 in human placentas which were obtained at normal delivery. The placentas were homogenized in a cold sucrose Tris-HCl buffer, pH 7.5. The microsomal fraction was incubated at 37 degrees C in air for 1 hr with 2 micrograms of T4 in the presence of 50mM DTT. The T3 and rT3 generated in the reaction mixture were extracted into cold ethanol and measured by RIA. Among the usal subcellular fractions of the placental homogenate, microsomes were the most potent in deiodinating T4 to rT3. In microsomes, production of rT3 increased with protein concentration, incubation temperature up to 37 degrees C, incubation time up to 120 min and T4 concentration up to 16 micrograms/tube. The production of rT3 from T4 was lost by prior heating of the microsomal fraction to 56 degrees C for 30 min. The net production rate of T4 to rT3 in the microsomal fraction was 17.9 ng/mg protein/micrograms T4/60 min at pH 7.5. RT3 production from T4 was maximal at pH 7.0. The production of T3 from T4 was negligible in the present system. Degradation of T3 in the placentas was rapid. Although the addition of anti-T3 antibody to the reaction mixture suppressed the degradation of T3, it had no effect on the net production of T3, suggesting that the obtained net T3 production rate had not been influenced by its degradation. Degradation of rT3 was negligible. These results indicate that the human placenta actively deiodinates T4 to rT3 enzymatically. This enzyme system might have some influence on the transplacental passage of the thyroid hormone from the mother to the fetus.

Female↗
PubMed1982

[Monodeiodination of thyroxine to 3,3', 5-triiodothyronine and 3,3', 5'-triiodothyronine in human kidney homogenate (author's transl)].

The renal cortex, later proved by histology to be free of carcinoma, was obtained from the kidneys of 9 patients undergoing nephrectomy for hypernephroma or ureteral carcinoma. The cortex was homogenized in a cold 50mM Tris-HCl buffer, pH 7.5, and centrifuged at 800 X g. Supernatants (1.8 mg protein, referred to as "homogenate") were enriched with 2 micrograms of T4 and were incubated for varying periods at different temperatures. The T3 and rT3 formed were extracted into ethanol and measured by RIA. Reaction mixtures contained 5mM dithiothreitol, without which formation of T3 and rT3 from T4 was negligible. The production of T3 and rT3 from T4 was abolished by prior heating of the homogenate to 56 degrees C for 30 min. In fresh homogenates, the production of T3 and rT3 increased with an increased concentration of homogenate (0.2-1.8 mg protein), increased incubation temperature up to 37 degrees C, increased incubation time up to 60 min, and increased T4 concentration up to 8 micrograms/tub. T3 production from T4 was near maximal at pH 6.5 and rT3 production at pH 10. At the standard pH of 7.5, rates of net T3 and rT3 production were 58 and 45%, respectively, of those at the optimum pH. Degradation of rT3 was rapid, while degradation of T3 was negligible. Both T3 and rT3 production from T4 were inhibited in a dose dependent manner by ipodate, propylthiouracil and salicylate. The apparent Km values for monodeiodination of T4 to T3 was 10 microM. Among the usual subcellular fractions of the kidney homogenate, microsomes were most potent in deiodinating T4 to T3 and to rT3. These results indicate that the human renal cortex contains the enzymes generating T3 and rT3 from T4.

Humans↗
PubMed1982

Serum free thyroxine and triiodothyronine concentrations in subacute thyroiditis.

Serum absolute free T4 (AFT4) and T3 (AFT3) concentrations were studied in 10 patients with subacute thyroiditis whose total serum T4 levels were elevated, and values were compared with those obtained in 10 patients with untreated Graves' disease, whose total serum T4 concentrations were elevated to the same level as in the former group. The mean (+/- SD) basal metabolic rate in patients with subacute thyroiditis was 16 +/- 14.8%, significantly (P less than 0.001) lower than that in patients with Graves' disease (48.7 +/- 15.7%). Serum T4-binding globulin concentrations measured by RIA were normal and did not differ from those in Graves' disease patients. The percentage of free T4 and AFT4 were both elevated in subacute thyroiditis to a degree comparable to that seen in Graves' disease. The serum total T3, serum free T3 fraction and AFT3 were also elevated, but both total T3 and AFT3 were significantly (P less than 0.05 and P less than 0.05, respectively) lower than in Graves' disease patients. Therefore, the ratios of T3 to T4 and AFT3 to AFT4 were significantly (P less than 0.01 and P less than 0.01, respectively) lower than in Graves' disease patients. These results indicate that the significantly lower basal metabolic rate and milder manifestations of thyrotoxic symptoms in subacute thyroiditis than in Graves' disease might be explained by the low ratios of T3 to T4 and AFT3 to AFT4 as well as the short duration of chemical hyperthyroidism.

Alpha-Globulins↗