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From:
Chris Betzold <[log in to unmask]>
Reply To:
Lactation Information and Discussion <[log in to unmask]>
Date:
Mon, 14 Mar 2005 22:35:38 EST
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FYI   Chris 
 
 
Eur J Endocrinol. 1995 Nov;133(5):613-7.
Usefulness of recombinant human prolactin for treatment of poor puerperal 
lactation in a rat model.

Yoneda N, Irahara M, Saito S, Uemura H, Aono T.

Department of Obstetrics and Gynecology, School of Medicine, University of 
Tokushima, Japan.

Recombinant human prolactin (r-hPRL) was produced by a line of murine C127 
cells transfected with human PRL gene. To assess the biological efficacy of 
r-hPRL in vivo, we studied its influence on milk secretion using a rat model in 
which lactation was reduced by bromocriptine treatment. Puerperal rats were 
injected daily for 9 days after delivery with bromocriptine or bromocriptine plus 
r-hPRL, and lactational performance was assessed by weighing the pups. The 
concentrations of rat and human PRL in rat serum were measured by specific 
radioimmunoassays and the mammary glands were examined on postpartum day 10. Daily 
injection of bromocriptine (0.1 mg/rat) significantly reduced the endogenous 
level of rat PRL and impaired the weight gain of the pups. Administration of 
r-hPRL increased the serum level of human PRL. Daily injections of r-hPRL (50 
micrograms/rat, twice a day) restored lactational performance and significantly 
increased the weight of the pups. The detrimental effect of bromocriptine on 
the mammary glands, assessed by both weight and histological appearance, was 
reversed by administration of r-hPRL. These results demonstrate that r-hPRL is 
biologically active in vivo and replacement therapy of r-hPRL is effective in 
improving the lactational performance in bromocriptine-treated rats, and also 
that r-hPRL may be useful for the treatment of women with poor lactation.

PMID: 7581993 [PubMed - indexed for MEDLINE] 

Christine Betzold NP IBCLC MSN

www.theBFclinic.com

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