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Bone Disorders

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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
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Proteins are broken down into amino acids during digestion. Unlike fats and carbohydrates, which are stored for later use, proteins are not. Instead, amino acids are either used to produce ATP through oxidation or contribute to the creation of new proteins for the growth and repair of the body. Any surplus amino acids from the diet are converted into glucose or triglycerides rather than excreted.
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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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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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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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Related Experiment Video

Updated: May 28, 2025

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
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Chrebp Deletion and Mild Protein Restriction Additively Decrease Muscle and Bone Mass and Function.

Kanako Deguchi1, Chihiro Ushiroda1, Shihomi Hidaka2

  • 1Department of Clinical Nutrition, Fujita Health University, Toyoake 470-1192, Japan.

Nutrients
|February 13, 2025
PubMed
Summary
This summary is machine-generated.

Mild protein restriction and carbohydrate response element binding protein (ChREBP) deletion negatively impact muscle and bone health. Maintaining adequate carbohydrate and protein intake is crucial for preserving muscle and bone mass and function.

Keywords:
bone mineral densitycarbohydratecarbohydrate binding proteinfatmuscle massprotein

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Area of Science:

  • Metabolic regulation
  • Nutritional science
  • Musculoskeletal health

Background:

  • Carbohydrate and protein restriction are linked to sarcopenia and osteopenia, but mechanisms are unclear.
  • Investigating the impact of mild protein restriction on muscle and bone in wild-type (WT) and ChREBP knockout (KO) mice.

Purpose of the Study:

  • To determine the effects of mild protein restriction on muscle and bone function in WT and ChREBP KO mice.
  • To elucidate the underlying mechanisms contributing to potential muscle and bone deficits.

Main Methods:

  • Eighteen-week-old male WT and ChREBP KO mice were fed control (20% protein) or low-protein (15% protein) diets for 12 weeks.
  • Assessed muscle weight, limb grip strength, bone mineral density (BMD), bone structure, and bone morphometry.

Main Results:

  • ChREBP deletion and low-protein diet additively decreased body weight, fat weight, muscle weight, and limb grip strength.
  • These muscle deficits were associated with decreased insulin/IGF-1 mRNA and increased myostatin mRNA.
  • ChREBP deletion increased BMD and bone structural integrity, but protein restriction in KO mice reversed these benefits, decreasing BMD and stiffness. Mild protein restriction reduced bone formation markers only in WT mice.

Conclusions:

  • Both ChREBP deletion and protein restriction impair muscle and bone function, suggesting a role for ChREBP in musculoskeletal health.
  • Adequate carbohydrate and protein intake is essential for maintaining muscle and bone mass and function.
  • Further research is needed to fully understand the mechanisms behind ChREBP deletion and low-protein diet-induced osteosarcopenia.