Document Detail


Has the mammary gland a protective mechanism against overexposure to triiodothyronine during the peripartum period? The prolactin pulse down-regulates mammary type I deiodinase responsiveness to norepinephrine.
MedLine Citation:
PMID:  15531715     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Peripartum is a crucial period for mammary gland final differentiation and the onset of lactation. Although the 'trigger' for lactogenesis depends on several hormones, a key factor is the peripartum prolactin (PRL) pulse whose deletion results in a failure to initiate milk production. Other hormones having a critical role during this period but exerting a contrary effect are the thyronines. A transitory hypothyroidism occurs at peripartum in serum and several other extrathyroidal tissues, whereas the induction of hyperthyroidism during late pregnancy is associated with the absence of lactation after delivery. We analyzed the mammary gland during pregnancy and lactation for: (a) the type and amount of thyroid receptors (TRs), (b) the local triiodothyronine (T3) generation catalyzed by type I deiodinase (Dio1), (c) the Dio1 response to norepinephrine (NE) and (d) the effect on Dio1 and TRs of blocking the PRL pulse at peripartum. Our data showed that during pregnancy the mammary gland contains Dio1 in low amounts associated with the highest expression of TRalpha1; whereas during lactation the gland shows high levels of both Dio1 and TRalpha1. However, at peripartum, both TRs and Dio1 decrease, and Dio1 becomes refractory to NE. This refractoriness disappears when the PRL pulse is blocked by the dopamine agonist bromocriptine. This blockade is also accompanied by a significant decrease in cyclin D1 expression. Our data suggested that the peripartum PRL pulse is part of a protective mechanism against precocious differentiation and/or premature involution of the alveolar epithelium due to T3 overexposure.
Authors:
B Anguiano; R Rojas-Huidobro; G Delgado; C Aceves
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of endocrinology     Volume:  183     ISSN:  0022-0795     ISO Abbreviation:  J. Endocrinol.     Publication Date:  2004 Nov 
Date Detail:
Created Date:  2004-11-08     Completed Date:  2005-02-01     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375363     Medline TA:  J Endocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  267-77     Citation Subset:  IM    
Affiliation:
Instituto de Neurobiología, UNAM-Juriquilla, Querétaro, México 76230.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cyclin D1 / metabolism
Female
Iodide Peroxidase / metabolism
Labor, Obstetric / metabolism*
Mammary Glands, Animal / drug effects,  metabolism*
Norepinephrine / pharmacology
Postpartum Period / metabolism*
Pregnancy
Prolactin / blood*
Rats
Rats, Sprague-Dawley
Stimulation, Chemical
Thyroid Hormone Receptors alpha / metabolism
Thyroid Hormone Receptors beta / metabolism
Triiodothyronine / metabolism*
Chemical
Reg. No./Substance:
0/Thyroid Hormone Receptors alpha; 0/Thyroid Hormone Receptors beta; 136601-57-5/Cyclin D1; 51-41-2/Norepinephrine; 6893-02-3/Triiodothyronine; 9002-62-4/Prolactin; EC 1.11.1.8/Iodide Peroxidase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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