<scp>l</scp>-THYROXINE AND 3,5,3’-TRII000-<scp>l</scp>-THYRONINE IN RAT EMBRYOS BEFORE ONSET OF FETAL THYROID FUNCTION.

Obregón, Marı́a Jesús; Mallol, J.; Pastor, Rosa María Ayela; Escobar, Gustavo; Rey, Francisco Escobar del

doi:10.1210/endo-114-1-305

Cited by 184 publications

(90 citation statements)

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“…Both T 4 and T 3 have been detected in rat embryo (20) and fetal rat brain (21) before the onset of fetal thyroid function. Morreale de Escobar et al (22) demonstrated that maternal hypothyroxinemia due to iodine deficiency resulted in lack of thyroid hormone in fetal tissues during early pregnancy, even before the onset of fetal thyroid function.…”

Section: Discussionmentioning

confidence: 99%

Endemic cretinism in Thailand: a multidisciplinary survey

Rajatanavin

Chailurkit²,

Winichakoon³

et al. 1997

European Journal of Endocrinology

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Endemic cretinism has been classified into neurological and myxedematous types. Profound mental deficiency, deaf-mutism and cerebral diplegia are predominantly found in the former. The latter have been described as less mentally retarded but with severe growth retardation and myxedematous features. The pathogenesis of different clinical types of endemic cretinism is still unclear. Recently, a unifying hypothesis suggested that iodine deficiency, severe enough to cause maternal and fetal hypothyroxinemia, results in neurological defects in all cretins.We conducted the present study in northern Thailand to determine the validity of this hypothesis in another geographical area. The study consisted of a multidisciplinary survey on 112 endemic cretins aged 2-66 years in Nan. They were categorized clinically into three types of endemic cretins, neurological (n = 57), myxedematous (n = 19) and mixed form (n = 36). The subjects were generally short and the majority had severe mental retardation (mean intellectual quotient (I.Q.) 30.8 Ϯ 8.8), psychomotor defect and profound sensorineural hearing loss. The I.Q. score and proportion of cretins with sensorineural hearing loss and psychomotor defect were similar among the three types of cretins. The most frequent neurological abnormalities were spasticity, hyper-reflexia, the presence of primitive reflexes and gait disturbance. These abnormalities were distributed equally among the three types of endemic cretins. Delayed skeletal maturation and abnormal epiphysis were also present in all types of cretins. However, myxedematous cretins were shorter (P < 0.01), having more myxedematous features (P < 0.05 to P<0.001) and less sexual maturation (P < 0.05). Thyroid volume was lower in cretins with hypothyroidism (P < 0.01).In conclusion, our findings support the hypothesis that neurological features are present in all types of cretins, and are the consequence of maternal and fetal hypothyroxinemia due to severe iodine deficiency. The clinical manifestations of the cretins were subsequently modified by the length and severity of postnatal iodine deficiency and hypothyroidism.

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Section: Discussionmentioning

confidence: 99%

Endemic cretinism in Thailand: a multidisciplinary survey

Rajatanavin

Chailurkit²,

Winichakoon³

et al. 1997

European Journal of Endocrinology

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“…In humans as well as in rodents, thyroid hormones as well as their receptors are present in the fetus prior to the onset of fetal thyroid hormone A c c e p t e d M a n u s c r i p t production underscoring the relevance of maternal thyroid hormone production for fetal development (Bernal and Pekonen, 1984;Obregón et al, 1984;Contempré et al, 1993;Morreale de Escobar et al, 2004). For instance, already at week 12 of gestation both T4 and T3 can be detected in the human developing cortex but not in the serum and other fetal tissues.…”

Section: Ontogenesis Of Thyroid Hormone Actionmentioning

confidence: 99%

Thyroid hormone action during brain development: More questions than answers

Horn

Heuer

2010

Molecular and Cellular Endocrinology

174

109

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“…However, microglial cells were already present in the developing rat brain at E12 (Ashwell, 1991;Sorokin et al, 1992), 4 d before the beginning of MTU treatment (E16). Early transplacental transfer of thyroid hormones from the mother (Obregon et al, 1984;Porterfield and Hendrich, 1992) therefore might have influenced the early fetal development of the microglial cells.…”

Section: Thyroid Hormone Favors Microglia Expansion: Early Postnatal mentioning

confidence: 99%

Regulation of Microglial Development: A Novel Role for Thyroid Hormone

et al. 2001

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The postnatal development of rat microglia is marked by an important increase in the number of microglial cells and the growth of their ramified processes. We studied the role of thyroid hormone in microglial development. The distribution and morphology of microglial cells stained with isolectin B4 or monoclonal antibody ED1 were analyzed in cortical and subcortical forebrain regions of developing rats rendered hypothyroid by prenatal and postnatal treatment with methyl-thiouracil. Microglial processes were markedly less abundant in hypothyroid pups than in age-matched normal animals, from postnatal day 4 up to the end of the third postnatal week of life. A delay in process extension and a decrease in the density of microglial cell bodies, as shown by cell counts in the developing cingulate cortex of normal and hypothyroid animals, were responsible for these differences. Conversely, neonatal rat hyperthyroidism, induced by daily injections of 3,5,3Ј-triiodothyronine (T3), accelerated the extension of microglial processes and increased the density of cortical microglial cell bodies above physiological levels during the first postnatal week of life.Reverse transcription-PCR and immunological analyses indicated that cultured cortical ameboid microglial cells expressed the ␣1 and ␤1 isoforms of nuclear thyroid hormone receptors. Consistent with the trophic and morphogenetic effects of thyroid hormone observed in situ, T3 favored the survival of cultured purified microglial cells and the growth of their processes. These results demonstrate that thyroid hormone promotes the growth and morphological differentiation of microglia during development.

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l-THYROXINE AND 3,5,3’-TRII000-l-THYRONINE IN RAT EMBRYOS BEFORE ONSET OF FETAL THYROID FUNCTION.

Cited by 184 publications

References 0 publications

Endemic cretinism in Thailand: a multidisciplinary survey

Endemic cretinism in Thailand: a multidisciplinary survey

Thyroid hormone action during brain development: More questions than answers

Regulation of Microglial Development: A Novel Role for Thyroid Hormone

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