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  • Author: T Hasegawa x
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Y. Fukiishi, T. Harauchi, T. Yoshizaki, Y. Hasegawa and Y. Eguchi


The ontogeny of thyroid peroxidase (TPO) activity was investigated in rat foetuses and neonates. From day 19 to 22 of gestation in intact pregnant rats, the TPO activity in their foetuses increased with foetal age.

Following maternal treatment with propylthiouracil (PTU), the TPO activity markedly increased in foetuses on and after day 20 of gestation. The TPO activity in encephalectomized foetuses increased as markedly as that in intact littermates, whereas that in hypophysectomized littermates failed to increase.

Newborn rats nursed by mothers treated with PTU had a TPO activity similar to that in controls of untreated mothers. There was also no difference in the TPO activity between hypophysectomized adult females and intact adult ones.

These observations show that in foetal rats, TPO activity increases disproportionately to the thyroid weight, but not in newborn and adult rats, and suggest that preferential synthesis of this enzyme occurs in addition to cell hypertrophy during foetal life.

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M Fukami, N Matsuo, T Hasegawa, S Sato and T Ogata

OBJECTIVE: To report on auxological data in the combination of SHOX (short stature homeobox containing gene) haploinsufficiency and normal ovarian function. DESIGN: Longitudinal auxological study in a 14 Year 9 Month old Japanese girl with Leri-Weill dyschondrosteosis accompanied by mesomelic short stature, who had a submicroscopic pseudoautosomal deletion involving SHOX, and pubertal development of an almost average tempo. METHODS: Auxological data were assessed by the age-matched standards for Japanese females. RESULTS: The standard deviation scores (SDSs) for height, leg length (LL), and arm span remained below the normal range from childhood and worsened during puberty, whereas those for sitting height (SH) remained within the normal range and stayed almost constant throughout the observation period. Consequently, the SDSs for SH/LL ratio remained above the normal range from childhood and deteriorated during puberty. The decreased pubertal height gain was caused by a diminished pubertal height spurt and abrupt growth cessation shortly after menarche. The SDSs for hand length and palm length remained within the normal range but decreased during puberty, and those for head circumference remained within the normal range and stayed almost constant throughout the observation period. CONCLUSIONS: The results suggest that, in individuals with SHOX haploinsufficiency and normal ovarian function, auxological abnormalities related to mesomelia are evident from childhood and worsen further during puberty because of the skeletal maturing effects of ovarian estrogens.

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Y. Hasegawa, T. Yoshida, Y. Fukiishi and Y. Mizushima


The potent synthetic glucocorticoid betamethasone 17,21-dipropionate (BMDP) produces adrenal hypertrophy in the rat foetus at late pregnancy by mediation of the hypothalamo-pituitary system, but causes adrenal atrophy, and acts as a normal glucocorticoid, in the adult rat. The change of the adrenal cortical response to the BMDP treatment was investigated in perinatal rat offspring. The pituitary ACTH potency was also determined in rat foetus treated with BMDP.

The time course of the adrenal corticosterone level after the BMDP treatment was similar to that of the plasma level on day 19 to 21 in the rat foetus from the adrenalectomized mother, both decreased at 2 h, but rose gradually at 4 h to 6 h, exceeding the control level at 24 h and 48 h after the BMDP treatment. The pituitary ACTH potency in the foetus decreased at 24 h and 48 h after the BMDP treatment, suggesting that ACTH released from the foetal pituitary stimulated adrenal corticoidogenesis. Maternal adrenalectomy did not essentially alter this stimulating activity of BMDP, which appeared in the perinatal rat offspring, only when BMDP was administered during the foetal period. These findings suggest that the hypothalamo-pituitary adrenocortical response to the treatment with BMDP drastically changes at the early neonatal age.

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T Ogata, K Muroya, H Ohashi, H Mochizuki, T Hasegawa and M Kaji

OBJECTIVE: A sex determining gene(s) has been mapped to a approximately 700 kb region distal to the exons of DMRT1 on 9p. The aim of this study was to examine gonadal developmental status in XX patients hemizygous for the 9p sex determining region. DESIGN: Clinical and molecular studies were performed in an 8-year-old girl with 46,XX,del(9)(p22) (case 1) and in a 2-year-old girl with 46,XX,del(9)(p23) (case 2). METHODS: Ovarian function status was assessed by gonadotrophin-releasing hormone (GnRH) tests. Hemizygosity for the sex determining region was examined by fluorescence in situ hybridisation and microsatellite analyses for a total of 17 loci on distal 9p. RESULTS: GnRH tests indicated mild gonadotrophin hyper responses in both cases (case 1: follicle stimulating hormone 9.2-->22.7 IU/l, luteinising hormone 0.7 --> 16.6 IU/l; case 2: follicle stimulating hormone 7.6 --> 38.2 IU/l, luteinising hormone 0.6 --> 9.4 IU/l). Molecular studies showed hemizygosity for the 9p sex determining region in both cases. CONCLUSIONS: The results, in conjunction with previous reports describing sex development in XX and XY patients hemizygous for the 9p sex determining region, imply that haploinsufficiency of the 9p sex determining gene(s) primarily hinders the formation of the indifferent gonad, leading to a wide range of testicular or ovarian development.

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Y Tang, H Osawa, H Onuma, M Hasegawa, T Nishimiya, M Ochi and H Makino

OBJECTIVE: Phosphodiesterase (PDE) 3B is a key enzyme involved in the anti-lipolytic action of insulin in adipocytes. PDE3B activation results in a reduced output of free fatty acids (FFA), whereas elevated serum FFA is known to cause insulin resistance. We have recently reported that reduced PDE3B gene expression is restored by treatment with pioglitazone, in the adipose tissues of obese, insulin-resistant diabetic KKAy mice. To determine whether the altered PDE3B gene expression is specific for adipocytes, the expression of this gene in liver and epididymal fat tissues of KKAy mice was examined. The effect of JTT-501, another peroxisome proliferator-activated receptor (PPAR)gamma ligand, which is different from thiazolidinedione, was also examined. METHODS: PDE3B mRNA and protein were quantified by an RNase protection assay and Western blotting respectively. Membrane-bound PDE activities were also measured. RESULTS: In adipose tissues of KKAy mice, PDE3B mRNA, protein and membrane-bound PDE activity were reduced to 47%, 57% and 51% respectively relative to those in C57BL/6J control mice. JTT-501 increased PDE3B mRNA, protein and membrane-bound PDE activity by 2.2-, 1.6- and 1.7-fold respectively over those of untreated KKAy mice. In the liver, PDE3B gene expression remained unchanged in KKAy mice, and was not affected by JTT-501. JTT-501 reduced the elevated levels of serum insulin, glucose, FFA and triglyceride in KKAy mice. CONCLUSIONS: PDE3B gene expression was specifically reduced in the adipose tissues of KKAy mice. JTT-501 restored this reduced gene expression with an accompanying improvement in elevated serum FFA and insulin resistance.