Bone changes due to pregnancy and lactation: influence of vitamin D status. | - CCMAR -

Journal Article

TitleBone changes due to pregnancy and lactation: influence of vitamin D status.
Publication TypeJournal Article
AuthorsMarie, PJ, M. Cancela, L, Le Boulch, N, Miravet, L
Year of Publication1986
JournalAm J Physiol
Volume251
Issue4 Pt 1
Date Published1986 Oct
PaginationE400-6
ISSN0002-9513
KeywordsAnimals, Bone and Bones, Bone Development, Bone Resorption, Calcitriol, Calcium, Female, Lactation, Minerals, Parathyroid Hormone, Phosphates, Pregnancy, Pregnancy, Animal, Rats, Vitamin D Deficiency
Abstract

The effects of pregnancy and lactation on endosteal bone formation and resorption were evaluated in vitamin D-depleted (-D) and vitamin D-repleted (+D) rats. Pregnancy induced a marked stimulation of osteoclastic bone resorption and of static and dynamic parameters of bone formation and mineralization. Bone resorption increased independently of vitamin D status and did not correlate with plasma 1,25-dihydroxyvitamin D3 [1,25(OH)2D] levels, but it was associated with increased plasma immunoreactive parathyroid hormone (iPTH) concentrations. Stimulation of the endosteal bone formation rate was mainly impaired in D-depleted rats, resulting in trabecular bone loss, which, in -D mother rats, was associated with decreased bone ash and total bone calcium. Lactation further stimulated bone resorption and reduced the trabecular bone volume; ash weight and bone calcium content were also decreased independently of the vitamin D status and changes in plasma iPTH levels. In presence of vitamin D, the bone formation rate increased fourfold during lactation but was unchanged in -D lactating rats. During lactation, vitamin D-depleted rats lost twofold more calcified bone than +D rats because of impaired mineralization. Thus, the present study shows that both the endosteal bone resorption and formation are stimulated by pregnancy and lactation and that vitamin D is required for normal bone mineralization during the reproductive period.

Sapientia

http://www.ncbi.nlm.nih.gov/pubmed/3766725?dopt=Abstract

Alternate JournalAm. J. Physiol.
PubMed ID3766725
CCMAR Authors