Gut Microbiota Modulates Obesity‐Associated Skeletal Deterioration Through Macrophage Aging and Grancalcin Secretion

Obesity is associated with skeletal deterioration and increased fracture risk, but the underlying mechanism is unclear. Herein, it is shown that obese gut microbiota promotes skeletal deterioration by inducing bone marrow macrophages (BMMs) senescence and grancalcin (GCA) secretion. Obese mice and t...

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Published inAdvanced science Vol. 12; no. 28; pp. e2502634 - n/a
Main Authors Huang, Min, Huang, Mei, Liu, Ling, Yang, Fang, He, Chen, Sun, Yu‐Chen, Jiao, Yu‐Rui, Tang, Xiang, Hou, Jing, Chen, Kai‐Xuan, He, Wen‐Zhen, Wei, Jie, Chen, Hui‐Ling, Li, Xia, Zeng, Chao, Lei, Guang‐Hua, Li, Chang‐Jun
Format Journal Article
LanguageEnglish
Published Germany John Wiley & Sons, Inc 01.07.2025
John Wiley and Sons Inc
Wiley
Subjects
Aging
Animals
Antibiotics
Bacteria
Bone marrow
Cellular Senescence
Chronic illnesses
Feces
Female
Fractures
Gastrointestinal Microbiome - physiology
Genes
Gram-negative bacteria
grancalcin
Gut microbiota
Homeostasis
Humans
Immune system
immunosenescence
Inflammation
Macrophages - metabolism
Male
Metabolic disorders
Mice
Mice, Inbred C57BL
Obesity
Obesity - complications
Obesity - metabolism
Obesity - microbiology
Senescence
Signal transduction
skeletal deterioration
gut‐microbiota
immunosenescence
grancalcin
skeletal deterioration
obesity
Online AccessGet full text
ISSN2198-3844
2198-3844
DOI10.1002/advs.202502634

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Abstract Obesity is associated with skeletal deterioration and increased fracture risk, but the underlying mechanism is unclear. Herein, it is shown that obese gut microbiota promotes skeletal deterioration by inducing bone marrow macrophages (BMMs) senescence and grancalcin (GCA) secretion. Obese mice and those receiving obese fecal microbiota transplants exhibit increased senescent macrophages and elevated GCA expression in the bone marrow. In a study of 40 participants, it is found that obese patients are associated with higher serum GCA levels. It is further revealed that obese gut‐microbiota derived lipopolysaccharides (LPS) stimulate GCA expression in senescent BMMs via activating Toll‐like receptor 4 pathway. Mice with depletion of the Gca gene are resistant to the negative effects of obesity and LPS on bone. Moreover, neutralizing antibody against GCA mitigates skeletal deterioration in obese mice and LPS‐induced chronic inflammation mouse model. The data suggest that the interaction between gut microbiota and the immune system contributes to obesity‐associated skeletal deterioration, and targeting senescent macrophages and GCA shows potential of protecting skeletal health in obese population. Obese gut‐microbiota derived lipopolysaccharides (LPS) induce bone marrow macrophage senescence and GCA secretion via activating TLR4/NF‐κB/MAPKs pathway. Clinically, obese patients are associated with higher serum GCA levels. Mice with depletion of GCA gene show resistance to skeletal deterioration caused by obesity and LPS‐induced chronic inflammation. GCA‐neutralizing antibody shows potential of ameliorating skeletal deterioration in obese and chronic inflammation mouse model.
AbstractList Obesity is associated with skeletal deterioration and increased fracture risk, but the underlying mechanism is unclear. Herein, it is shown that obese gut microbiota promotes skeletal deterioration by inducing bone marrow macrophages (BMMs) senescence and grancalcin (GCA) secretion. Obese mice and those receiving obese fecal microbiota transplants exhibit increased senescent macrophages and elevated GCA expression in the bone marrow. In a study of 40 participants, it is found that obese patients are associated with higher serum GCA levels. It is further revealed that obese gut-microbiota derived lipopolysaccharides (LPS) stimulate GCA expression in senescent BMMs via activating Toll-like receptor 4 pathway. Mice with depletion of the Gca gene are resistant to the negative effects of obesity and LPS on bone. Moreover, neutralizing antibody against GCA mitigates skeletal deterioration in obese mice and LPS-induced chronic inflammation mouse model. The data suggest that the interaction between gut microbiota and the immune system contributes to obesity-associated skeletal deterioration, and targeting senescent macrophages and GCA shows potential of protecting skeletal health in obese population.
Obesity is associated with skeletal deterioration and increased fracture risk, but the underlying mechanism is unclear. Herein, it is shown that obese gut microbiota promotes skeletal deterioration by inducing bone marrow macrophages (BMMs) senescence and grancalcin (GCA) secretion. Obese mice and those receiving obese fecal microbiota transplants exhibit increased senescent macrophages and elevated GCA expression in the bone marrow. In a study of 40 participants, it is found that obese patients are associated with higher serum GCA levels. It is further revealed that obese gut‐microbiota derived lipopolysaccharides (LPS) stimulate GCA expression in senescent BMMs via activating Toll‐like receptor 4 pathway. Mice with depletion of the Gca gene are resistant to the negative effects of obesity and LPS on bone. Moreover, neutralizing antibody against GCA mitigates skeletal deterioration in obese mice and LPS‐induced chronic inflammation mouse model. The data suggest that the interaction between gut microbiota and the immune system contributes to obesity‐associated skeletal deterioration, and targeting senescent macrophages and GCA shows potential of protecting skeletal health in obese population. Obese gut‐microbiota derived lipopolysaccharides (LPS) induce bone marrow macrophage senescence and GCA secretion via activating TLR4/NF‐κB/MAPKs pathway. Clinically, obese patients are associated with higher serum GCA levels. Mice with depletion of GCA gene show resistance to skeletal deterioration caused by obesity and LPS‐induced chronic inflammation. GCA‐neutralizing antibody shows potential of ameliorating skeletal deterioration in obese and chronic inflammation mouse model.
Abstract Obesity is associated with skeletal deterioration and increased fracture risk, but the underlying mechanism is unclear. Herein, it is shown that obese gut microbiota promotes skeletal deterioration by inducing bone marrow macrophages (BMMs) senescence and grancalcin (GCA) secretion. Obese mice and those receiving obese fecal microbiota transplants exhibit increased senescent macrophages and elevated GCA expression in the bone marrow. In a study of 40 participants, it is found that obese patients are associated with higher serum GCA levels. It is further revealed that obese gut‐microbiota derived lipopolysaccharides (LPS) stimulate GCA expression in senescent BMMs via activating Toll‐like receptor 4 pathway. Mice with depletion of the Gca gene are resistant to the negative effects of obesity and LPS on bone. Moreover, neutralizing antibody against GCA mitigates skeletal deterioration in obese mice and LPS‐induced chronic inflammation mouse model. The data suggest that the interaction between gut microbiota and the immune system contributes to obesity‐associated skeletal deterioration, and targeting senescent macrophages and GCA shows potential of protecting skeletal health in obese population.
Obesity is associated with skeletal deterioration and increased fracture risk, but the underlying mechanism is unclear. Herein, it is shown that obese gut microbiota promotes skeletal deterioration by inducing bone marrow macrophages (BMMs) senescence and grancalcin (GCA) secretion. Obese mice and those receiving obese fecal microbiota transplants exhibit increased senescent macrophages and elevated GCA expression in the bone marrow. In a study of 40 participants, it is found that obese patients are associated with higher serum GCA levels. It is further revealed that obese gut‐microbiota derived lipopolysaccharides (LPS) stimulate GCA expression in senescent BMMs via activating Toll‐like receptor 4 pathway. Mice with depletion of the Gca gene are resistant to the negative effects of obesity and LPS on bone. Moreover, neutralizing antibody against GCA mitigates skeletal deterioration in obese mice and LPS‐induced chronic inflammation mouse model. The data suggest that the interaction between gut microbiota and the immune system contributes to obesity‐associated skeletal deterioration, and targeting senescent macrophages and GCA shows potential of protecting skeletal health in obese population. Obese gut‐microbiota derived lipopolysaccharides (LPS) induce bone marrow macrophage senescence and GCA secretion via activating TLR4/NF‐κB/MAPKs pathway. Clinically, obese patients are associated with higher serum GCA levels. Mice with depletion of GCA gene show resistance to skeletal deterioration caused by obesity and LPS‐induced chronic inflammation. GCA‐neutralizing antibody shows potential of ameliorating skeletal deterioration in obese and chronic inflammation mouse model.
Obesity is associated with skeletal deterioration and increased fracture risk, but the underlying mechanism is unclear. Herein, it is shown that obese gut microbiota promotes skeletal deterioration by inducing bone marrow macrophages (BMMs) senescence and grancalcin (GCA) secretion. Obese mice and those receiving obese fecal microbiota transplants exhibit increased senescent macrophages and elevated GCA expression in the bone marrow. In a study of 40 participants, it is found that obese patients are associated with higher serum GCA levels. It is further revealed that obese gut-microbiota derived lipopolysaccharides (LPS) stimulate GCA expression in senescent BMMs via activating Toll-like receptor 4 pathway. Mice with depletion of the Gca gene are resistant to the negative effects of obesity and LPS on bone. Moreover, neutralizing antibody against GCA mitigates skeletal deterioration in obese mice and LPS-induced chronic inflammation mouse model. The data suggest that the interaction between gut microbiota and the immune system contributes to obesity-associated skeletal deterioration, and targeting senescent macrophages and GCA shows potential of protecting skeletal health in obese population.Obesity is associated with skeletal deterioration and increased fracture risk, but the underlying mechanism is unclear. Herein, it is shown that obese gut microbiota promotes skeletal deterioration by inducing bone marrow macrophages (BMMs) senescence and grancalcin (GCA) secretion. Obese mice and those receiving obese fecal microbiota transplants exhibit increased senescent macrophages and elevated GCA expression in the bone marrow. In a study of 40 participants, it is found that obese patients are associated with higher serum GCA levels. It is further revealed that obese gut-microbiota derived lipopolysaccharides (LPS) stimulate GCA expression in senescent BMMs via activating Toll-like receptor 4 pathway. Mice with depletion of the Gca gene are resistant to the negative effects of obesity and LPS on bone. Moreover, neutralizing antibody against GCA mitigates skeletal deterioration in obese mice and LPS-induced chronic inflammation mouse model. The data suggest that the interaction between gut microbiota and the immune system contributes to obesity-associated skeletal deterioration, and targeting senescent macrophages and GCA shows potential of protecting skeletal health in obese population.
Author Chen, Kai‐Xuan
Liu, Ling
Li, Chang‐Jun
Zeng, Chao
Hou, Jing
He, Wen‐Zhen
Wei, Jie
Chen, Hui‐Ling
Lei, Guang‐Hua
Jiao, Yu‐Rui
Sun, Yu‐Chen
Tang, Xiang
Yang, Fang
Huang, Mei
Huang, Min
He, Chen
Li, Xia
AuthorAffiliation 5 Department of Orthopaedics Xiangya Hospital Central South University Changsha 410008 China
6 Department of Epidemiology and Health Statistics Xiangya School of Public Health Central South University Changsha 410008 China
1 Department of Endocrinology Endocrinology Research Center Xiangya Hospital Central South University Changsha 410008 China
10 FuRong Laboratory Changsha 410008 China
11 Laboratory Animal Center Xiangya Hospital Central South University Changsha 410008 China
4 Hunan Key Laboratory of Joint Degeneration and Injury Changsha 410008 China
8 Department of Endocrine Subspecialty of Gerontology Xiangya Hospital, Central South University Changsha 410008 China
2 Department of General Medicine The Fifth Affiliated Hospital of Xinjiang Medical University Urumqi 830000 China
7 Key Laboratory of Aging‐related Bone and Joint Diseases Prevention and Treatment Ministry of Education Xiangya Hospital Central South University Changsha 410008 China
3 Department of Clinical Laboratory Xiangya Hos
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Issue 28
Keywords gut‐microbiota
immunosenescence
grancalcin
skeletal deterioration
obesity
Language English
License Attribution
2025 The Author(s). Advanced Science published by Wiley‐VCH GmbH.
This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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Snippet Obesity is associated with skeletal deterioration and increased fracture risk, but the underlying mechanism is unclear. Herein, it is shown that obese gut...
Abstract Obesity is associated with skeletal deterioration and increased fracture risk, but the underlying mechanism is unclear. Herein, it is shown that obese...
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StartPage e2502634
SubjectTerms Aging
Animals
Antibiotics
Bacteria
Bone marrow
Cellular Senescence
Chronic illnesses
Feces
Female
Fractures
Gastrointestinal Microbiome - physiology
Genes
Gram-negative bacteria
grancalcin
Gut microbiota
Homeostasis
Humans
Immune system
immunosenescence
Inflammation
Macrophages - metabolism
Male
Metabolic disorders
Mice
Mice, Inbred C57BL
Obesity
Obesity - complications
Obesity - metabolism
Obesity - microbiology
Senescence
Signal transduction
skeletal deterioration
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Title Gut Microbiota Modulates Obesity‐Associated Skeletal Deterioration Through Macrophage Aging and Grancalcin Secretion
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