Maternal-Fetal Thyroid Interactions

Ahmed, R G

doi:10.5772/48076

Cited by 7 publications

(9 citation statements)

References 169 publications

(219 reference statements)

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“…These results can be due to the higher transfer of THs from pregnant females to their fetuses during pregnancy and/or more efficiency of thyroid gland to produce THs after birth (Jiskra et al, 2007;Ahmed et al, 2008;El-bakry et al, 2010;Ahmed, 2012a). The transplacental transport may also require deiodinases, transporters, sulfotransferases, and genomic and non-genomic actions (Loubière et al, 2010;Ahmed, 2011Ahmed, , 2012b. Several investigators El-bakry et al, 2010;Ahmed, 2011Ahmed, , 2012a stated that the gradual increase of TSH is necessary for the development of thyroid gland during this sensitive period.…”

Section: Discussionmentioning

confidence: 99%

“…We recently reported that thyroid functions during the development are dynamic and many external factors (i.e. dioxin) potentially influence the maternal-fetal-hypothalamic-pituitary-thyroid axis (HPTA) (Ahmed, 2011;Ahmed, 2012b). This result is reinforced by Madanat et al (2007) (2012) who undertook that higher serum TSH concentrations are generally associated with an increased risk of thyroid cancer.…”

Section: Discussionmentioning

confidence: 99%

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Gestational doxorubicin alters fetal thyroid–brain axis

Ahmed

Incerpi²

2012

Intl J of Devlp Neuroscience

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Administration of chemotherapy during pregnancy may represent a big risk factor for the developing brain, therefore we studied whether the transplacental transport of doxorubicin (DOX) may affect the development of neuroendocrine system. DOX (25 mg/kg; 3 times interaperitoneally/week) was given to pregnant rats during whole gestation period. The disturbances in neuroendocrine functions were investigated at gestation day (GD) 15 and 20 by following the maternal and fetal thyroid hormone levels, fetal nucleotides (ATP, ADP, AMP) levels and adenosine triphosphatase (Na(+), K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase) activities in two brain regions, cerebrum and cerebellum. In control group, the levels of maternal and fetal serum thyroxine (T4), triiodothyronine (T3), thyrotropin (TSH), and fetal serum growth hormone (GH) increased from days 15 to 20, whereas in the DOX group, a decrease in maternal and fetal T4, T3 and increase in TSH levels (hypothyroid status) were observed. Also, the levels of fetal GH decreased continuously from GD 15 to 20 with respect to control group. In cerebrum and cerebellum, the levels of fetal nucleotides and the activities of fetal ATPases in control group followed a synchronized course of development. The fetal hypothyroidism due to maternal administration of DOX decreased the levels of nucleotides, ATPases activities, and total adenylate, instead, the adenylate energy charge showed a trend to an increase in both brain regions at all ages tested. These alterations were dose- and age-dependent and this, in turn, may impair the nerve transmission. Finally, DOX may act as neuroendocrine disruptor causing hypothyroidism and fetal brain energetic dysfunction.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Gestational doxorubicin alters fetal thyroid–brain axis

Ahmed

Incerpi²

2012

Intl J of Devlp Neuroscience

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“…In fact, the most severe neurologic injury resulting from a thyroid deficiency is in endemic cretinism initiated by iodine deficiency [4,25,26]. During the first gestational trimester, maternal hypo-thyroxinemia limits the possibilities of postnatal neurodevelopment [27][28][29][30][31][32][33][34][35][36][37]. The most serious form of brain lesion links to neurological cretinism, but mild degrees of maternal hypo-thyroxinemia also produce variations in psychomotor development [38][39][40][41].…”

Section: Maternal Iodine Deficiencymentioning

confidence: 99%

“…Neuronal outgrowth and cellular migration are dependent on normal microtubule synthesis and assembly and these latter processes are regulated by THs [4,49]. During fetal and neonatal development, hypothyroidism results in delayed neuronal differentiation and diminished neuronal connectivity [33][34][35][36][37]49]. Interestingly, deficient cellular maturation in the cerebral cortex of hypothyroid rats is characterized by [4,50] the following: (a) Smaller neuronal cell bodies that are more tightly packed than those in euthyroid animals; (b) Diminished axonal and dendritic outgrowth, elongation, and branching; (c) Reduced numbers of dendritic spines.…”

Section: Th Deficiency and Neuronal Developmentmentioning

confidence: 99%

Maternal Iodine Deficiency and Brain Disorders

Rg¹

2016

Endocrinol Metab Syndr

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Thyroid Hormones (THs) play an essential role in development and hormone deficiency during critical phases in fetal life may lead to severe and permanent brain damage. Maternal iodine deficiency is considered the most common cause of fetal TH deficiency, but the problem may also arise in the fetus/neonates. Due to defects in fetal thyroid gland development or hormone synthesis, clinical symptoms at birth are often mild as a result of compensatory maternal TH supply. A shortage of THs starting at the early stages of pregnancy results in neurological deficits that cannot be rescued by exogenous TH addition at later stages. Neonates are more sensitive than adults to the effects of iodine deficiency. Thus, these disturbances may lead to abnormalities in the neuronal network and may result in mental retardation and other neurological defects, including impaired motor skills and visual processing. Thus, iodine defenses programmes can avoid adverse neurodevelopmental consequences in mothers and their offspring.

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“…The actions of THs are facilitated genomically by thyroid receptors (TRs, α and β) and non-genomically at the plasma membrane, in the cytoplasm and in cellular organelles [4,[49][50][51][52][53][54][55], by stimulation of Na+, K+, Ca2+ and glucose transport, activation of protein kinase C (PKC), protein kinase A (PKA) and mitogen activated and protein kinase (ERK/MAPK) [4]. In addition, the transport of T4 and T3 in and out of cells is controlled by several classes of transmembrane TH-transporters (THTs) [56], including members of the organic anion transporter family (OATP), L-type amino acid transporters (LATs), Na+/Taurocholate cotransporting polypeptide (NTCP), and monocarboxylate transporters (MCTs) [4,49,57,58]. Adding additional complexity, the metabolism of T4 and T3 is regulated by 3 selenoenzyme iodothyronine deiodinases (Ds: D1, D2 and D3) [59][60][61].…”

mentioning

confidence: 99%

Untitled

2017

Insights Biol Med

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CommunicationThe normal levels of thyroid hormones (THs; thyroxine, T4 & 3,5,3′-triiodo-Lthyronine, T3) are necessary for the normal development , particularly the fetal and neonatal cardiac growth and development [49]. The actions of THs are facilitated genomically by thyroid receptors (TRs, α and β) and non-genomically at the plasma membrane, in the cytoplasm and in cellular organelles [4,[49][50][51][52][53][54][55], by stimulation of Na+, K+, Ca2+ and glucose transport, activation of protein kinase C (PKC), protein kinase A (PKA) and mitogen activated and protein kinase (ERK/MAPK) [4]. In addition, the transport of T4 and T3 in and out of cells is controlled by several classes of transmembrane TH-transporters (THTs) [56], including members of the organic anion transporter family (OATP), L-type amino acid transporters (LATs), Na+/Taurocholate cotransporting polypeptide (NTCP), and monocarboxylate transporters (MCTs) [4,49,57,58]. Adding additional complexity, the metabolism of T4 and T3 is regulated by 3 selenoenzyme iodothyronine deiodinases (Ds: D1, D2 and D3) [59][60][61]. On the other hand, the congenital hypothyroidism can cause the following [49,[62][63][64], (1) congenital heart diseases; (2) diastolic hypertension; (3) reduced cardiac output, stroke volume and a narrow pulse pressure; (4) dilatation and overt heart failure; (5) elevation in the systemic vascular resistance [65][66][67][68]. Similarly, the chronic hyperthyroidism can cause the following [49,64]: (1) cardiac hypertrophy; (2) increase in the cardiomyocyte (CM) length rather than width; (3) noticeable diminution in systemic vascular resistance; (4) elevation in the cardiac contractility; (5) systolic hypertension; (6) increase in the cardiac output, venous volume return, blood volume and pulse pressure; and (7) reduction in the systemic vascular resistance [49,69]. T3-therapy can induce DNA synthesis and cardiomyocyte proliferation, and improve the cardiac contractility; though, this action is as still unidenti ied [49,[70][71][72][73][74].On the basis of these data, it can be reported that the T3 may stimulate the cardiac contractility and stimulate the hemodynamic changes (blood pressure, blood volume and heart rate) during the prenatal and postnatal periods. Additional studies are necessary to delineate the likely relations with human health. Future examinations are necessary to explore the multidirectional actions of TH-therapy in the maternal and neonatal cardiovascular diseases.

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Maternal-Fetal Thyroid Interactions

Cited by 7 publications

References 169 publications

Gestational doxorubicin alters fetal thyroid–brain axis

Gestational doxorubicin alters fetal thyroid–brain axis

Maternal Iodine Deficiency and Brain Disorders

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