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I Bonomo, Physiological Sciences, State University of Rio de Janeiro, RJ, Brazil
P Lisboa, Physiology Sciences, State University of Rio de Janeiro, Rio de Janeiro, Brazil
M Passos, State University of Rio de Janeiro, Rio de Janeiro, Brazil
S Alves, Rio de Janeiro, Brazil
A Reis, ICB, Federal University of Minas Gerais, MG, Brazil
E Moura, Physiological Sciences, State University of Rio de Janeiro, RJ, Brazil

Correspondence: Patricia Lisboa, Email: pclisboa{at}uerj.br

Abstract

Malnutrition during lactation is associated with hypoprolactinaemia and failure in milk production. Adult rats whose mothers were malnourished presented higher body weight and serum T3. Maternal hypoprolactinaemia at the end of lactation caused higher body weight at adult life, suggesting an association of maternal prolactin (PRL) level and programming of the adult offspring's body weight. Here, we studied the consequences of the maternal PRL inhibition at the end of lactation by bromocriptine (BRO) injection, a dopaminergic agonist, upon serum TSH and thyroid hormones, thyroid iodide uptake, liver mitochondrial alpha-glycerophosphate dehydrogenase (mGPD), liver and pituitary deiodinases activities (D1 and/or D2) and 'in vitro' post-TRH TSH release in the adult offspring. Wistar lactating rats were divided into: BRO- injected with 1mg/twice a day, daily for the last 3 days of lactation and C- control, saline-injected with the same frequency. At 180 days old, the offspring were injected with 125I ip and after 2h, they were sacrificed. Adult animals whose mothers were treated with BRO at the end of lactation presented lower serum TSH (-51%), T3 (-23%) and T4 (-21%), lower thyroid 125I uptake (-41%), liver mGPD (-55%) and pituitary D2 (-51%) activities, without changes in the 'in vitro' post-TRH TSH release. We evidenced that maternal PRL supression at the end of lactation programs a hypometabolic state in adulthood, in part due to a thyroid hypofunction, caused by a central hypothyroidism, probably due to decreased TRH secretion. We suggest that PRL during lactation can regulate the hypothalamus-pituitary-thyroid axis and programs its function.

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