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J Endocrinol. 2015 Mar;224(3):315-25. doi: 10.1530/JOE-14-0473. Epub 2015 Feb 4.

Effects of maternal nicotine exposure on thyroid hormone metabolism and function in adult rat progeny.

Author information

1
Laboratory of Endocrine PhysiologyLaboratory of NeurophysiologyBiology Institute, State University of Rio de Janeiro, Rio de Janeiro 20551-030, BrazilCarlos Chagas Filho Biophysic InstituteFederal University of Rio de Janeiro, Rio de Janeiro 21949-900, Brazil.
2
Laboratory of Endocrine PhysiologyLaboratory of NeurophysiologyBiology Institute, State University of Rio de Janeiro, Rio de Janeiro 20551-030, BrazilCarlos Chagas Filho Biophysic InstituteFederal University of Rio de Janeiro, Rio de Janeiro 21949-900, Brazil elainedeoliveir@yahoo.com.br elainedeoliveir@pq.cnpq.br.
3
Laboratory of Endocrine PhysiologyLaboratory of NeurophysiologyBiology Institute, State University of Rio de Janeiro, Rio de Janeiro 20551-030, BrazilCarlos Chagas Filho Biophysic InstituteFederal University of Rio de Janeiro, Rio de Janeiro 21949-900, Brazil Laboratory of Endocrine PhysiologyLaboratory of NeurophysiologyBiology Institute, State University of Rio de Janeiro, Rio de Janeiro 20551-030, BrazilCarlos Chagas Filho Biophysic InstituteFederal University of Rio de Janeiro, Rio de Janeiro 21949-900, Brazil.

Abstract

Postnatal nicotine exposure leads to obesity and hypothyroidism in adulthood. We studied the effects of maternal nicotine exposure during lactation on thyroid hormone (TH) metabolism and function in adult offspring. Lactating rats received implants of osmotic minipumps releasing nicotine (NIC, 6 mg/kg per day s.c.) or saline (control) from postnatal days 2 to 16. Offspring were killed at 180 days. We measured types 1 and 2 deiodinase activity and mRNA, mitochondrial α-glycerol-3-phosphate dehydrogenase (mGPD) activity, TH receptor (TR), uncoupling protein 1 (UCP1), hypothalamic TRH, pituitary TSH, and in vitro TRH-stimulated TSH secretion. Expression of deiodinase mRNAs followed the same profile as that of the enzymatic activity. NIC exposure caused lower 5'-D1 and mGPD activities; lower TRβ1 content in liver as well as lower 5'-D1 activity in muscle; and higher 5'-D2 activity in brown adipose tissue (BAT), heart, and testis, which are in accordance with hypothyroidism. Although deiodinase activities were not changed in the hypothalamus, pituitary, and thyroid of NIC offspring, UCP1 expression was lower in BAT. Levels of both TRH and TSH were lower in offspring exposed to NIC, which presented higher basal in vitro TSH secretion, which was not increased in response to TRH. Thus, the hypothyroidism in NIC offspring at adulthood was caused, in part, by in vivo TRH-TSH suppression and lower sensitivity to TRH. Despite the hypothyroid status of peripheral tissues, these animals seem to develop an adaptive mechanism to preserve thyroxine to triiodothyronine conversion in central tissues.

KEYWORDS:

TH receptor; TSH; deiodinase; lactation; nicotine; programing; thyroid hormones; α-glycerol-3-phosphate dehydrogenase

PMID:
25653393
DOI:
10.1530/JOE-14-0473
[Indexed for MEDLINE]

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