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Related Concept Videos

Hormones and Bone Tissue01:17

Hormones and Bone Tissue

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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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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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Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormones. Communication between the gut and brain via vagal nerve fibers plays a significant role in evaluating the contents of the gut. Clinical studies have shown that protein ingestion produces a more prolonged response in these nerve fibers compared to an equivalent amount of glucose. Additionally, the activation of stretch receptors caused by GI...
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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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Related Experiment Video

Updated: Nov 18, 2025

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
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Decrease in leptin mediates rat bone metabolism impairments during high-fat diet-induced catch-up growth by

Xiaoling Liu1, Yuzhen Liang2, Ning Xia1

  • 1Department of Endocrinology and Metabolism, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021 People's Republic of China.

3 Biotech
|February 8, 2021
PubMed
Summary

High-fat diets induce catch-up growth (CUG), impairing bone metabolism. Leptin and its antagonist significantly altered bone markers, with leptin influencing osteoprotegerin (OPG) and receptor activator of nuclear factor-kappa b ligand (RANKL) during CUG.

Keywords:
Bone metabolismCatch-up growthHigh-fat dietLeptinOPGRANKL

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Area of Science:

  • Endocrinology
  • Bone Biology
  • Metabolic Research

Background:

  • Catch-up growth (CUG) has known adverse health effects, but its impact on bone metabolism remains under-investigated.
  • High-fat diets (HFD) are a common trigger for CUG, necessitating research into associated metabolic consequences.
  • Leptin's role in bone metabolism during CUG requires clarification, particularly in the context of HFD.

Purpose of the Study:

  • To investigate the effects of leptin on bone metabolism and formation during high-fat diet-induced catch-up growth.
  • To elucidate the mechanisms involving leptin, osteoprotegerin (OPG), and receptor activator of nuclear factor-kappa b ligand (RANKL) in HFD-induced CUG bone changes.

Main Methods:

  • Male Wistar rats were divided into control, caloric restriction/normal chow, caloric restriction/HFD, and HFD/leptin antagonist groups.
  • Body weight, biochemical markers, and adipose tissue were monitored.
  • Bone metabolism was assessed using Hematoxylin and Eosin (H&E) staining, qRT-PCR, and immunohistochemistry for OPG and RANKL.

Main Results:

  • HFD significantly increased body weight and adipose tissue accumulation.
  • Bone metabolism markers were significantly altered in the caloric restriction/HFD and HFD/leptin antagonist groups.
  • HFD-induced CUG led to severe bone formation impairment, exacerbated by a leptin antagonist, with decreased OPG and increased RANKL expression.

Conclusions:

  • High-fat diet-induced catch-up growth significantly impairs bone formation.
  • Leptin plays a crucial role in regulating bone metabolism during HFD-induced CUG, mediated by OPG and RANKL.
  • Leptin antagonism during CUG further aggravates bone loss, highlighting leptin's protective role in bone health under these conditions.