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Related Experiment Video

Updated: Jul 6, 2026

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

Published on: March 15, 2018

High d(+)glucose concentration inhibits RANKL-induced osteoclastogenesis.

Y Wittrant¹, Y Gorin, K Woodruff

¹Department of Pathology, University of Texas Health Science Center, and South Texas Veteran's Health Care System, Audie L. Murphy Division, San Antonio, TX 78229, USA. wittrant@uthscsa.edu

|April 2, 2008

Summary

High glucose levels in diabetes inhibit osteoclast formation and function, impacting bone metabolism. This study reveals glucose

Related Experiment Videos

Last Updated: Jul 6, 2026

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

Published on: March 15, 2018

Area of Science:

Endocrinology
Bone Biology
Metabolic Diseases

Background:

Diabetes mellitus is linked to bone complications like osteoporosis and fractures.
Hyperglycemia's role in diabetic bone disease pathogenesis, particularly osteoclastogenesis, remains unclear.
Understanding glucose's direct effects on bone cells is crucial for managing diabetic bone complications.

Purpose of the Study:

To investigate the impact of high d-glucose (d-Glc) on RANKL-induced osteoclastogenesis in vitro.
To elucidate the underlying mechanisms, including reactive oxygen species (ROS) and Nuclear Factor kappaB (NF-kappaB) signaling.
To assess the effect of high glucose on osteoclast cellular functions like migration.

Main Methods:

Utilized RAW264.7 cells and Bone Marrow Macrophages (BMM) as models for osteoclastogenesis.
Exposed cells to sustained high d-Glc and l-Glc (osmotic control) mimicking diabetic conditions.
Assessed osteoclast formation, gene expression (CTR, cathepsin K), ROS production, caspase-3 and NF-kappaB activity, and cell migration.

Main Results:

High d-Glc significantly inhibited osteoclast formation, ROS production, caspase-3 activity, and cell migration.
Findings suggest high d-Glc alters osteoclastogenesis via a metabolic pathway.
High d-Glc may inhibit redox-sensitive NF-kappaB activity through an anti-oxidative mechanism.

Conclusions:

High glucose levels decrease osteoclast differentiation and function, potentially altering bone turnover in diabetes.
This study provides novel insights into the biologic effects of glucose on osteoclastogenesis.
Results highlight a potential mechanism contributing to diabetes-associated bone disease.