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¹ Departamento de Ciências Fisiológicas - 5o andar, Instituto de Biologia Roberto Alcântara Gomes² Departamento de Nutrição Aplicada, Instituto de Nutrição, Universidade do Estado do Rio de Janeiro, Avenida 28 de setembro, 87, Rio de Janeiro, RJ 20551-030, Brazil³ Departamento de Fisiologia e Biofísica, ICB, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil

(Correspondence should be addressed to E G de Moura; Email: egberto{at}pq.cnpq.br)

Malnutrition during lactation is associated with hypoprolactinemia and failure in milk production. Adult rats whose mothers were malnourished presented higher body weight and serum tri-iodothyronine (T₃). Maternal hypoprolactinemia at the end of lactation caused higher body weight in adult life, suggesting an association between maternal prolactin (PRL) level and programming of the offspring's adult 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 -glycerophosphate dehydrogenase (mGPD), liver and pituitary de-iodinase 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 1 mg/twice a day, daily for the last 3 days of lactation, and C – control, saline-injected with the same frequency. At 180 days of age, the offspring were injected with ¹²⁵I i.p. and after 2 h, they were killed. Adult animals whose mothers were treated with BRO at the end of lactation presented lower serum TSH (–51%), T₃ (–23%), and thyroxine (–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 show that maternal PRL suppression 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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