Skeletal changes during lactation and after weaning in osteocyte-specific sclerostin overexpressed mice

Su Jin Lee, Sun Yong Song, Yumie Rhee

Research output: Contribution to journalArticle

Abstract

Introduction: Lactation inevitably leads to a state of rapid bone loss; however, maternal bone undergoes rapid remineralization after weaning. Sclerostin, encoded by the gene SOST, is exclusively secreted from osteocytes and plays important roles in bone remodeling. However, there are few studies about the effect of sclerostin during lactation and weaning on bone microstructures. Therefore, we conducted the study to demonstrate any possible association of sclerostin with bone metabolism and skeletal changes during lactation and after weaning. Materials and methods: We analyzed bone mineral density (BMD) by dual-energy X-ray absorptiometry at the spine and femur, bone microstructure by micro-computed tomography (μCT) at the distal and mid-shaft of the femur and biochemical markers such as sclerostin and bone turnover markers at 1 week and 3 weeks of lactation and 2 weeks post-weaning in osteocyte-specific sclerostin-overexpressed transgenic mice, and compared them with wild type. Results: Lactation significantly resulted in decreased spine and femur BMD at day 7 and day 21 of breastfeeding; specifically, cortical microstructure (cross-sectional thickness and cross-sectional area) at the mid-shaft of the femur had significantly deteriorated. At day 14 after weaning, femur BMD and cortical microstructure at the mid-shaft of the femur in both the wild and DMP-SOST mice had incompletely recovered; however, spine BMD and trabecular microstructures at the distal femur recovered in wild type mice. Conclusions: Sclerostin, secreted by osteocytes, played a role in bone loss during lactation and also in the recovery of trabecular bone compartment by activating bone formation after weaning.

Original languageEnglish
JournalJournal of Bone and Mineral Metabolism
DOIs
Publication statusAccepted/In press - 2019 Jan 1

Fingerprint

Osteocytes
Weaning
Lactation
Femur
Bone and Bones
Bone Density
Spine
Bone Remodeling
Photon Absorptiometry
Breast Feeding
Osteogenesis
Transgenic Mice
Biomarkers
Tomography
Mothers
Genes

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Orthopedics and Sports Medicine
  • Endocrinology

Cite this

@article{e541610844374fcba41dd8bf7f0aa31b,
title = "Skeletal changes during lactation and after weaning in osteocyte-specific sclerostin overexpressed mice",
abstract = "Introduction: Lactation inevitably leads to a state of rapid bone loss; however, maternal bone undergoes rapid remineralization after weaning. Sclerostin, encoded by the gene SOST, is exclusively secreted from osteocytes and plays important roles in bone remodeling. However, there are few studies about the effect of sclerostin during lactation and weaning on bone microstructures. Therefore, we conducted the study to demonstrate any possible association of sclerostin with bone metabolism and skeletal changes during lactation and after weaning. Materials and methods: We analyzed bone mineral density (BMD) by dual-energy X-ray absorptiometry at the spine and femur, bone microstructure by micro-computed tomography (μCT) at the distal and mid-shaft of the femur and biochemical markers such as sclerostin and bone turnover markers at 1 week and 3 weeks of lactation and 2 weeks post-weaning in osteocyte-specific sclerostin-overexpressed transgenic mice, and compared them with wild type. Results: Lactation significantly resulted in decreased spine and femur BMD at day 7 and day 21 of breastfeeding; specifically, cortical microstructure (cross-sectional thickness and cross-sectional area) at the mid-shaft of the femur had significantly deteriorated. At day 14 after weaning, femur BMD and cortical microstructure at the mid-shaft of the femur in both the wild and DMP-SOST mice had incompletely recovered; however, spine BMD and trabecular microstructures at the distal femur recovered in wild type mice. Conclusions: Sclerostin, secreted by osteocytes, played a role in bone loss during lactation and also in the recovery of trabecular bone compartment by activating bone formation after weaning.",
author = "Lee, {Su Jin} and Song, {Sun Yong} and Yumie Rhee",
year = "2019",
month = "1",
day = "1",
doi = "10.1007/s00774-019-01044-6",
language = "English",
journal = "Journal of Bone and Mineral Metabolism",
issn = "0914-8779",
publisher = "Springer Japan",

}

TY - JOUR

T1 - Skeletal changes during lactation and after weaning in osteocyte-specific sclerostin overexpressed mice

AU - Lee, Su Jin

AU - Song, Sun Yong

AU - Rhee, Yumie

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Introduction: Lactation inevitably leads to a state of rapid bone loss; however, maternal bone undergoes rapid remineralization after weaning. Sclerostin, encoded by the gene SOST, is exclusively secreted from osteocytes and plays important roles in bone remodeling. However, there are few studies about the effect of sclerostin during lactation and weaning on bone microstructures. Therefore, we conducted the study to demonstrate any possible association of sclerostin with bone metabolism and skeletal changes during lactation and after weaning. Materials and methods: We analyzed bone mineral density (BMD) by dual-energy X-ray absorptiometry at the spine and femur, bone microstructure by micro-computed tomography (μCT) at the distal and mid-shaft of the femur and biochemical markers such as sclerostin and bone turnover markers at 1 week and 3 weeks of lactation and 2 weeks post-weaning in osteocyte-specific sclerostin-overexpressed transgenic mice, and compared them with wild type. Results: Lactation significantly resulted in decreased spine and femur BMD at day 7 and day 21 of breastfeeding; specifically, cortical microstructure (cross-sectional thickness and cross-sectional area) at the mid-shaft of the femur had significantly deteriorated. At day 14 after weaning, femur BMD and cortical microstructure at the mid-shaft of the femur in both the wild and DMP-SOST mice had incompletely recovered; however, spine BMD and trabecular microstructures at the distal femur recovered in wild type mice. Conclusions: Sclerostin, secreted by osteocytes, played a role in bone loss during lactation and also in the recovery of trabecular bone compartment by activating bone formation after weaning.

AB - Introduction: Lactation inevitably leads to a state of rapid bone loss; however, maternal bone undergoes rapid remineralization after weaning. Sclerostin, encoded by the gene SOST, is exclusively secreted from osteocytes and plays important roles in bone remodeling. However, there are few studies about the effect of sclerostin during lactation and weaning on bone microstructures. Therefore, we conducted the study to demonstrate any possible association of sclerostin with bone metabolism and skeletal changes during lactation and after weaning. Materials and methods: We analyzed bone mineral density (BMD) by dual-energy X-ray absorptiometry at the spine and femur, bone microstructure by micro-computed tomography (μCT) at the distal and mid-shaft of the femur and biochemical markers such as sclerostin and bone turnover markers at 1 week and 3 weeks of lactation and 2 weeks post-weaning in osteocyte-specific sclerostin-overexpressed transgenic mice, and compared them with wild type. Results: Lactation significantly resulted in decreased spine and femur BMD at day 7 and day 21 of breastfeeding; specifically, cortical microstructure (cross-sectional thickness and cross-sectional area) at the mid-shaft of the femur had significantly deteriorated. At day 14 after weaning, femur BMD and cortical microstructure at the mid-shaft of the femur in both the wild and DMP-SOST mice had incompletely recovered; however, spine BMD and trabecular microstructures at the distal femur recovered in wild type mice. Conclusions: Sclerostin, secreted by osteocytes, played a role in bone loss during lactation and also in the recovery of trabecular bone compartment by activating bone formation after weaning.

UR - http://www.scopus.com/inward/record.url?scp=85073982280&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85073982280&partnerID=8YFLogxK

U2 - 10.1007/s00774-019-01044-6

DO - 10.1007/s00774-019-01044-6

M3 - Article

C2 - 31501981

AN - SCOPUS:85073982280

JO - Journal of Bone and Mineral Metabolism

JF - Journal of Bone and Mineral Metabolism

SN - 0914-8779

ER -