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Related Concept Videos

Bone Remodeling01:40

Bone Remodeling

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Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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Hormones and Bone Tissue01:17

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The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
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TGF - β Signaling Pathway01:16

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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Covalently Linked Protein Regulators02:04

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Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
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The Parathyroid Glands00:59

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The two pairs of parathyroid glands embedded within the posterior surface of the thyroid gland are restricted by a dense capsule around them. These glands comprise two distinct cell populations—parathyroid oxyphil and parathyroid principal cells- pivotal in calcium homeostasis.
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Related Experiment Video

Updated: Mar 17, 2026

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
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PPARG Post-translational Modifications Regulate Bone Formation and Bone Resorption.

L A Stechschulte1, P J Czernik2, Z C Rotter2

  • 1Dept. Orthopaedic Surgery, University of Toledo Health Science Campus, Toledo, OH 43614, United States; Center for Diabetes and Endocrine Research, University of Toledo Health Science Campus, Toledo, OH 43614, United States.

Ebiomedicine
|July 17, 2016
PubMed
Summary
This summary is machine-generated.

New research shows that targeting peroxisome proliferator-activated receptor gamma (PPARγ) with SR10171 can improve bone density and metabolic health. This suggests a potential treatment for both diabetes and bone disease.

Keywords:
AdipocyteBoneInsulin sensitizersOsteoblastOsteoclastOsteocytePPARγPost-translational modifications

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Area of Science:

  • Molecular endocrinology
  • Metabolic bone disease
  • Diabetes research

Background:

  • Peroxisome proliferator-activated receptor gamma (PPARγ) is a key regulator of bone cell differentiation and a target for insulin-sensitizing drugs (TZDs).
  • Thiazolidinediones (TZDs) improve glucose metabolism but are associated with bone loss and fracture risk, limiting their clinical use.
  • Post-translational modifications at S112 and S273 influence PPARγ's effects on adipogenesis, insulin sensitivity, and potentially bone metabolism.

Purpose of the Study:

  • To investigate the role of PPARγ post-translational modifications (pS112 and pS273) in regulating both bone and metabolic parameters.
  • To evaluate the therapeutic potential of selectively targeting PPARγ activity for treating metabolic and bone diseases simultaneously.

Main Methods:

  • Treatment of hyperglycemic and normoglycemic animal models with SR10171, a selective inverse agonist for pS273.
  • Assessment of bone parameters, including trabecular and cortical bone mass.
  • Evaluation of metabolic parameters and bone cell activities (osteocyte, osteoblast, osteoclast) and marrow adiposity.

Main Results:

  • SR10171 treatment significantly increased trabecular and cortical bone mass in animal models.
  • The drug normalized metabolic parameters without affecting pS112 activity.
  • SR10171 modulated osteocyte, osteoblast, and osteoclast activities, and reduced marrow adiposity.

Conclusions:

  • Specific post-translational modifications of PPARγ differentially regulate bone and metabolic functions.
  • Selective inhibition of pS273 with SR10171 improves bone mass and metabolic health.
  • This suggests a unified therapeutic strategy targeting both diabetes and metabolic bone disease through PPARγ modulation.