M Kodama

Kumamoto University, Kumamoto, Kumamoto Prefecture, Japan

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Publications (7)13.06 Total impact

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    ABSTRACT: OBJECTIVES Our previous studies demonstrated autonomic nervous system disorders and cerebral blood hypoperfusion in school refusal students with underlying emotional distress due to fear or anxiety associated with school attendance. Because severe stress is known to affect glucoregulatory metabolism, this study used the oral glucose tolerance test (OGTT) to measure glucose metabolism in school refusal students.DESIGNA three-hour OGTT was performed. In preparation for the test, students fasted overnight. After a fasting blood sample was drawn, students were given solutions containing a predetermined amount of glucose based on their body weight (1.75 g/kg to a maximum 75 g). After glucose ingestion, blood samples were drawn at 30, 60, 90, 120, 150, and 180 min to measure blood glucose (BG), immunoreactive insulin (IRI), pancreatic glucagon (IRG) and growth hormone (GH) levels. BG levels, IRI response, cumulative BG (ΣBG), cumulative IRI (ΣIRI), insulin/glucose ratio (ΔIRI/ΔBG), and insulinogenic index (ΣIRI/ΣBG) were then compared to previously reported normal control data. As an index of emotional difficulties, the self-rating depressive scale (SDS) was carried out.PATIENTSEighty-one school refusal students (40 males and 41 females), 11–19 years of age (14.8 ± 2.1), were studied. Their school refusal periods ranged from one month to eight years. All students were within – 15 to + 20 %(-0.04 ± 8.6) of ideal body weight.MEASUREMENTSBG levels were determined using a glucose oxidase reaction method. Serum hormones were measured by radioimmunoassay.RESULTSBG levels at all OGTT time intervals and ΣBG were significantly higher in school refusal students than the normal control data (ΣBG: 39.5 ± 4.4 vs 33.3 ± 3.4 mmol/l, P < 0.001). Although the insulin response was abnormally low relative to the prevailing hyperglycaemia (ΣIRI/ΣBG: subjects vs control = 232 ± 129 vs 375 ± 271, P < 0.01), normal beta cell secretory ability was speculated (ΣIRI: subjects vs controls = 2805 ± 1274 vs 2523 ± 1219 pmol/l). This suggests a relative suppression of insulin secretion. A paradoxical increase of GH was observed in 19 students after glucose ingestion.CONCLUSIONS Glucoregulatory disorders observed in school refusal students may be caused by emotional distress. Multiple factors including autonomic nervous system disorders, derangement of neuropeptides in the hypothalamus, and hormonal imbalances may also affect glucoregulatory metabolism, predisposing these students to hyperglycaemia. We speculate that the glucoregulatory system compensates for decreased blood flow to the brain by increasing blood glucose concentrations, thereby providing sufficient glucose as the primary energy source used during normal brain metabolism.
    Clinical Endocrinology 10/2003; 47(3):273 - 278. · 3.40 Impact Factor
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    ABSTRACT: Thyroid transcription factor-1 encoded by the NKX2.1 gene is a candidate regulator of thyroid and lung morphogenesis and function in humans. We report 2 female siblings with congenital thyroid dysfunction and recurrent acute respiratory distress carrying a heterozygous deletion of chromosome 14q12-13.3, resulting in haploinsufficiency for the NKX2.1 gene. This observation further supports a physiologic role for thyroid transcription factor-1 in early human thyroid and pulmonary function.
    Journal of Pediatrics 09/2000; 137(2):272-6. · 4.04 Impact Factor
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    ABSTRACT: Our previous studies demonstrated autonomic nervous system disorders and cerebral blood hypoperfusion in school refusal students with underlying emotional distress due to fear or anxiety associated with school attendance. Because severe stress is known to affect glucoregulatory metabolism, this study used the oral glucose tolerance test (OGTT) to measure glucose metabolism in school refusal students. A three-hour OGTT was performed. In preparation for the test, students fasted overnight. After a fasting blood sample was drawn, students were given solutions containing a predetermined amount of glucose based on their body weight (1.75 g/kg to a maximum 75 g). After glucose ingestion, blood samples were drawn at 30, 60, 90, 120, 150, and 180 mm to measure blood glucose (BG), immunoreactive insulin (IRI), pancreatic glucagon (IRG) and growth hormone (GH) levels. BG levels, IRI response, cumulative BG (sigma BG), cumulative IRI (sigma IRI), insulin/glucose ratio (delta IRI/delta BG), and insulinogenic index (sigma IRI/sigma BG) were then compared to previously reported normal control data. As an index of emotional difficulties, the self-rating depressive scale (SDS) was carried out. Eighty-one school refusal students (40 males and 41 females), 11-19 years of age (14.8 +/- 2.1), were studied. Their school refusal periods ranged from one month to eight years. All students were within -15 to +20% (-0.04 +/- 8.6) of ideal body weight. BG levels were determined using a glucose oxidase reaction method. Serum hormones were measured by radioimmunoassay. BG levels at all OGTT time intervals and sigma BG were significantly higher in school refusal students than the normal control data (sigma BG: 39.5 +/- 4.4 vs 33.3 +/- 3.4 mmol/l P < 0.001). Although the insulin response was abnormally low relative to the prevailing hyperglycaemia (sigma IRI/ sigma BG: subjects vs control = 232 +/- 129 vs 375 +/- 271, P < 0.01), normal beta cell secretory ability was speculated (sigma IRI: subjects vs controls = 2805 +/- 1274 vs 2523 +/- 1219 pmol/l). This suggests a relative suppression of insulin secretion. A paradoxical increase of GH was observed in 19 students after glucose ingestion. Glucoregulatory disorders observed in school refusal students may be caused by emotional distress. Multiple factors including autonomic nervous system disorders, derangement of neuropeptides in the hypothalamus, and hormonal imbalances may also affect glucoregulatory metabolism, predisposing these students to hyperglycaemia. We speculate that the glucoregulatory system compensates for decreased blood flow to the brain by increasing blood glucose concentrations, thereby providing sufficient glucose as the primary energy source used during normal brain metabolism.
    Clinical Endocrinology 09/1997; 47(3):273-8. · 3.40 Impact Factor
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    ABSTRACT: Deletions and point mutations of the growth hormone (GH) receptor gene (GHR) have been identified in patients with Laron syndrome. We report the first detection of the GHR mutation among Japanese patients with Laron syndrome. Using the Japanese female patient's genomic DNA as a template, all exons and flanking portions of introns of GHR were amplified by polymerase chain reaction (PCR). Sequencing of the PCR products showed that the patient was homozygous for a G to A substitution at the first position of intron 4. This substitution was same as that detected in a Spanish patient and a north European patient. The base change occurred at the 5' splice consensus sequence of intron 4, resulting in the abolition of a BanI restriction site. Since this substitution was not detected by a BanI restriction analysis in 85 control individuals, it is more likely a disease-related splice mutation than a polymorphism. The mutation in our patient was predicted to destroy the original 5' splice site of intron 4 of GHR and to produce a new cryptic splice site, leading to abnormal mRNA processing and a lack of GH binding activity of GH-binding protein (GHBP).
    The Japanese journal of human genetics 07/1997; 42(2):323-9.
  • N Iwatani, M Kodama, T Miike
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    ABSTRACT: Three growth hormone (GH) deficient males with hypogonadotropic hypogonadism were treated with pulsatile luteinizing hormone-releasing hormone (LH-RH) administration. In two of them, the GH deficiency was idiopathic, but in the other it was secondary, caused by suprasellar germinoma. In response to LH-RH therapy, the serum testosterone (T), testicular volume, and body height increased in all three patients, and normal serum T levels and spermatogenesis were achieved in two patients. Gonadotropin responses to an LH-RH test preceding therapy did not seem to be an accurate predictor of the success of LH-RH therapy. We conclude that GH-deficient patients with hypogonadotropic hypogonadism can be expected to achieve normal pubertal development and spermatogenesis with pulsatile LH-RH administration.
    Endocrine Journal 05/1993; 40(2):191-6. · 2.23 Impact Factor
  • N Iwatani, M Kodama, H Seto
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    ABSTRACT: We describe a female child with pituitary gigantism and precocious adrenarche. From two years of age she showed unusual overgrowth, and at 5 years old she was 133.5 cm (+ 5.5 SD) tall and weighed 40.5 kg. Her precocious manifestations were public hair, acne vulgaris, hirsutism, and advanced bone age. Endocrinological examination revealed markedly increased serum growth hormone (GH) and prolactin (PRL), which responded paradoxically to a TRH test. In addition, the concentrations of serum dehydroepiandrosterone (DHA) and its sulfate (DHAS) were increased to adult levels, moving in accordance with changes in ACTH, which suggested that these androgens were secreted from the adrenal glands functionally. These androgens seemed to be responsible for her partial precocity. Prior reports have suggested that GH and/or PRL overproduction might have played a role in the induction of adrenarche. Also, in previous reports of 9 gigantism patients under 10 years old, the manifestation of precocious adrenarche was suggested in 8. Further investigation of the influence of GH and PRL on adrenal androgen production in children with pituitary gigantism is required. On the other hand, in short children with normal GH secretion, attention should be paid to whether or not the GH therapy in early childhood induces precocious adrenarche.
    Endocrinologia japonica 07/1992; 39(3):251-7.
  • N Iwatani, M Kodama, T Miike
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    ABSTRACT: In this report we describe the first case of a girl with acromegaloidism in Japan. She had large and coarse facial features with acral enlargement accompanying height overgrowth; these resemble the manifestations of acromegaly and gigantism due to growth hormone (GH) overproduction. However, pituitary function studies revealed a dysfunction of her GH secretion. Moreover, markedly decreased serum somatomedin C (SM-C) levels also indicated impairment of GH secretion. Therefore, GH and SM-C cannot have been responsible for promoting somatic growth. However, serum alkaline-phosphatase (Al-P) and osteocalcin, were increased, indicating that stimulation of bone metabolism was increased without GH and SM-C effects. The patient is a typical case showing growth without GH, and these data suggest the existence of an unidentified growth promoting factor that is independent of GH and SM-C.
    Endocrinologia japonica 03/1992; 39(1):59-64.