title: Prolactin inhibition at the end of lactation programs for a central hypothyroidism in adult rat.
abstract: 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 (T(3)). 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 alpha-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 (125)I 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%), T(3) (-23%), and thyroxine (-21%), lower thyroid (125)I 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.
authors.affiliation: Departamento de Ciências Fisiológicas - 5o andar, Instituto de Biologia Roberto Alcântara Gomes, Instituto de Nutrição, Universidade do Estado do Rio de Janeiro, Avenida 28 de setembro, 87, Rio de Janeiro, RJ 20551-030, Brazil.
authors.forename: Isabela Teixeira
authors.initials: IT
authors.lastname: Bonomo
authors.forename: Patrícia Cristina
authors.initials: PC
authors.lastname: Lisboa
authors.forename: Magna Cottini Fonseca
authors.initials: MC
authors.lastname: Passos
authors.forename: Simone Bezerra
authors.initials: SB
authors.lastname: Alves
authors.forename: Adelina Martha
authors.initials: AM
authors.lastname: Reis
authors.forename: Egberto Gaspar
authors.initials: EG
authors.lastname: de Moura
mesh_terms: D000818:Animals; D001835:Body Weight / Q000187:drug effects; D001971:Bromocriptine / Q000494:pharmacology*; D004435:Eating; D005260:Female; D005993:Glycerolphosphate Dehydrogenase / Q000378:metabolism; D006727:Hormone Antagonists; D006966:Hyperprolactinemia / Q000097:blood / Q000139:chemically induced / Q000503:physiopathology; D007037:Hypothyroidism / Q000097:blood* / Q000139:chemically induced / Q000503:physiopathology*; D007453:Iodide Peroxidase / Q000378:metabolism; D007774:Lactation / Q000097:blood* / Q000187:drug effects*; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D039382:Maternal Nutritional Physiological Phenomena; D010902:Pituitary Gland / Q000187:drug effects / Q000201:enzymology; D011388:Prolactin / Q000037:antagonists & inhibitors*; D051381:Rats; D017208:Rats, Wistar; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D006727:Hormone Antagonists; D014284:Triiodothyronine; D001971:Bromocriptine; D011388:Prolactin; D013972:Thyrotropin; D005993:Glycerolphosphate Dehydrogenase; D007453:Iodide Peroxidase; D013974:Thyroxine