Perinatal and chronic hypothyroidism impair behavioural development in male and female rats

Wijk, Nick van; Rijntjes, Eddy; Heijning, Bert J. M. van de

doi:10.1113/expphysiol.2008.042416

Cited by 58 publications

(34 citation statements)

References 51 publications

(119 reference statements)

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“…Body temperature was significantly decreased in the hypothyroid offspring by 1.3°C from the start of measurements at day 28 postpartum. The observed reduction in body temperature of the hypothyroid rats was in line with earlier studies (53,57).…”

Section: Resultssupporting

confidence: 80%

Prenatal induced chronic dietary hypothyroidism delays but does not block adult-type Leydig cell development

Rijntjes

Swarts²,

Anand‐Ivell³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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Rijntjes E, Swarts HJ, Anand-Ivell R, Teerds KJ. Prenatal induced chronic dietary hypothyroidism delays but does not block adult-type Leydig cell development. Am J Physiol Endocrinol Metab 296: E305-E314, 2009. First published November 25, 2008 doi:10.1152/ajpendo.90750.2008.-Transient hypothyroidism induced by propyl-2-thiouracyl blocks postpartum Leydig cell development. In the present study, the effects of chronic hypothyroidism on the formation of this adult-type Leydig cell population were investigated, using a more physiological approach. Before mating, dams were put on a diet consisting of an iodide-poor feed supplemented with a low dose of perchlorate and, with their offspring, were kept on this diet until death. In the pups at day 12 postpartum, plasma thyroid-stimulating hormone levels were increased by 20-fold, whereas thyroxine and free tri-iodothyronine levels were severely depressed, confirming a hypothyroid condition. Adult-type progenitor Leydig cell formation and proliferation were reduced by 40 -60% on days 16 and 28 postpartum. This was followed by increased Leydig cell proliferation at later ages, suggesting a possible slower developmental onset of the adult-type Leydig cell population under hypothyroid conditions. Testosterone levels were increased 2-to 10-fold in the hypothyroid animals between days 21 and 42 postpartum compared with the age-matched controls. Combined with the decreased presence of 5␣-reductase, this implicates a lower production capacity of 5␣-reduced androgens. In 84-day-old rats, after correction for body weight-to-testis weight ratio, plasma insulin-like factor-3 levels were 35% lower in the hypothyroid animals, suggestive of a reduced Leydig cell population. This is confirmed by a 37% reduction in the Sertoli cell-to-Leydig cell ratio in hypothyroid rats. In conclusion, we show that dietary-induced hypothyroidism delays but, unlike propyl-2-thiouracyl, does not block the development of the adult-type Leydig cell population.

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Section: Resultssupporting

confidence: 80%

Prenatal induced chronic dietary hypothyroidism delays but does not block adult-type Leydig cell development

Rijntjes

Swarts²,

Anand‐Ivell³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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“…Such an association is also consistent with experimental studies showing the effects of chronic hypothyroidism on development (31). Overtreatment should also be avoided (32,33).…”

Section: Cognition Behavior and Socioeducational Attainmentsupporting

confidence: 70%

ENDOCRINOLOGY AND ADOLESCENCE: Congenital hypothyroidism: a clinical update of long-term outcome in young adults

Léger

2015

European Journal of Endocrinology

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Congenital hypothyroidism (CH) is the most common congenital endocrine disorder. The early treatment of CH patients has successfully improved the prognosis and management of this disorder. Optimal treatment and management throughout the patient's life, beginning in the neonatal period, are required to ensure long-term health. Affected patients should be offered assessments of associated medical conditions and provided with accurate information about their condition throughout their lives, but particularly during the transition from pediatric to adult services. This review provides a summary of current knowledge about the long-term outcomes of these patients and appropriate management into early adulthood. We carried out a systematic search of the Medline database to identify relevant articles. Despite major improvements in prognosis, the impact of CH is clearly not uniform, and management should take into account a broader range of relevant indicators, including CH severity, associated comorbid conditions and the adequacy of treatment during childhood and adulthood. The early diagnosis and management of associated medical conditions, and better educational strategies to improve compliance with treatment, should improve the long-term prognosis. Further studies are required to explore changes with aging.

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“…We tested the hypothesis that developmental ID and hypothyroidism may cause spatial learning impairments through a CaM-dependent pathway, which is supported by the literature. Indeed, hypothyroidism has well been identified to cause synaptic function deficits Dong et al 2005;Gerges et al 2005Gerges et al , 2001Gilbert et al 2007;Sui and Gilbert 2003;Sui et al 2005) and some gene expressions (Royland et al 2008) and impairs spatial learning and memory in the hippocampus by using adult animal models (Alzoubi et al 2009;Gilbert and Sui 2006;van Wijk et al 2008). Furthermore, PTU exposure leads to an irreversible dose-dependent learning deficits on spatial learning tasks (Gilbert and Sui 2006).…”

Section: Discussionmentioning

confidence: 96%

Developmental Iodine Deficiency and Hypothyroidism Impair Spatial Memory in Adolescent Rat Hippocampus: Involvement of CaMKII, Calmodulin and Calcineurin

et al. 2009

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Developmental iodine deficiency (ID) leads to inadequate thyroid hormone that impairs learning and memory with an unclear mechanism. Here, we show that hippocampal calcium/calmodulin-dependent protein kinase II (CaMKII), calmodulin and calcineurin are implicated in the impaired spatial memory in adolescent rats following developmental ID and hypothyroidism. Three developmental rat models were created by administrating dam rats with either iodine-deficient diet or propylthiouracil (PTU, 5 or 15 ppm)-added drinking water from gestational day (GD) 6 till postnatal day (PN) 28. Then, the spatial memory to a water maze test was studied in pups before PN42. After testing periods, the latency to platform and the number of error in iodine-deficient and 15 ppm PTU-treatment groups were significantly higher than those in the controls (P < 0.05). Total and phosphorylated CaMKII, calmodulin, and calcineurin in the hippocampus were detected with both the immunohistochemistry and western blotting. Without going through water maze test, iodine-deficient and 15 ppm PTU-treatment groups showed significantly lower CaMKII and calmodulin and significantly higher calcineurin than the controls in hippocampal CA1 and CA3 regions (P < 0.05). After trials of water maze task, however, CaMKII and calmodulin were up-regulated and calcineurin was down-regulated in control group (P < 0.05), but not in iodine-deficient and 15 ppm PTU-treatment groups. Data indicate that hippocampal CaMKII, calmodulin, and calcineurin are involved in the impaired spatial memory induced by developmental ID and hypothyroidism.

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Perinatal and chronic hypothyroidism impair behavioural development in male and female rats

Cited by 58 publications

References 51 publications

Prenatal induced chronic dietary hypothyroidism delays but does not block adult-type Leydig cell development

Prenatal induced chronic dietary hypothyroidism delays but does not block adult-type Leydig cell development

ENDOCRINOLOGY AND ADOLESCENCE: Congenital hypothyroidism: a clinical update of long-term outcome in young adults

Developmental Iodine Deficiency and Hypothyroidism Impair Spatial Memory in Adolescent Rat Hippocampus: Involvement of CaMKII, Calmodulin and Calcineurin

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