Zn glycine attenuates LPS-induced inflammatory bone loss in geese through suppression of osteoclastogenesis via reducing TLR-4/NFκB signaling

Lipopolysaccharide (LPS), a major component of the outer membrane of gram-negative bacteria such as Escherichia coli, disrupts gut microbial homeostasis, compromises intestinal barrier integrity, and contributes to inflammation-associated bone loss. Although the gut-bone axis is increasingly recognized as a critical regulator of skeletal health, effective nutritional strategies targeting this pathway remain insufficiently explored. This study investigated the protective effects of Zn glycine, a highly bioavailable organic zinc chelates, against LPS-induced inflammatory bone loss in meat geese. Dietary supplementation with Zn glycine at 80 mg/kg significantly alleviated LPS-induced growth impairment, intestinal barrier dysfunction. Zn glycine markedly reduced LPS accumulation in both intestinal and bone tissues (p < 0.01) and enhanced tight junction integrity by upregulating zonula occludens-1 and claudin-1, thereby limiting systemic LPS translocation. These effects were accompanied by reduced pro-inflammatory cytokines (IL-1β, IL-18, and TNF-α), elevated anti-inflammatory cytokine IL-10, and increased microbial production of short-chain fatty acids, collectively supporting gut and bone health. Additionally, Zn glycine mitigated LPS-induced oxidative stress by enhancing antioxidant enzyme activities and total antioxidant capacity while reducing oxidative damage markers. Importantly, Zn glycine preserved bone microarchitecture, increased (p < 0.01) bone mineral density (BMD), suppressed osteoclastic genes such as tumor necrosis factor receptor-associated factor 6 (TRAF6) and nuclear factor of activated T-cells cytoplasmic 1 (NFATC1), and promoted osteoblast activity through upregulation of runt-related transcription factor 2 (RUNX2), osteocalcin (OCN), and alkaline phosphatase (ALP). Mechanistically, these protective effects were mediated through inhibition of the TLR4/NF-κB signaling pathway. Overall, Zn glycine emerges as a promising nutritional strategy for preventing inflammation-driven bone loss via modulation of the gut-bone axis.

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Publication Details

Journal
Ecotoxicology and Environmental Safety
Published
2026-01-01
DOI
https://doi.org/10.1016/j.ecoenv.2025.119655
Citations
1
Primary Topic
Bone Metabolism and Diseases
Type
article
Field-Weighted Citation Impact
22.24
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article

Zn glycine attenuates LPS-induced inflammatory bone loss in geese through suppression of osteoclastogenesis via reducing TLR-4/NFκB signaling

Yalei Cui, Aftab Shaukat, Boshuai Liu, Layla Al-Mitib et al.
1 citations
Ecotoxicology and Environmental Safety
Bone Metabolism and Diseases
22.24
article

Zn glycine attenuates LPS-induced inflammatory bone loss in geese through suppression of osteoclastogenesis via reducing TLR-4/NFκB signaling

Yalei Cui, Aftab Shaukat, Boshuai Liu, Layla Al-Mitib, Hao Sun, Muhammad Arslan Asif, Waseem Abbas, Zeshan ZULFİQAR, Yinghua Shi, Xiaoyan Zhu, Zhichang Wang
article en
1 citations

Abstract

Lipopolysaccharide (LPS), a major component of the outer membrane of gram-negative bacteria such as Escherichia coli, disrupts gut microbial homeostasis, compromises intestinal barrier integrity, and contributes to inflammation-associated bone loss. Although the gut-bone axis is increasingly recognized as a critical regulator of skeletal health, effective nutritional strategies targeting this pathway remain insufficiently explored. This study investigated the protective effects of Zn glycine, a highly bioavailable organic zinc chelates, against LPS-induced inflammatory bone loss in meat geese. Dietary supplementation with Zn glycine at 80 mg/kg significantly alleviated LPS-induced growth impairment, intestinal barrier dysfunction. Zn glycine markedly reduced LPS accumulation in both intestinal and bone tissues (p < 0.01) and enhanced tight junction integrity by upregulating zonula occludens-1 and claudin-1, thereby limiting systemic LPS translocation. These effects were accompanied by reduced pro-inflammatory cytokines (IL-1β, IL-18, and TNF-α), elevated anti-inflammatory cytokine IL-10, and increased microbial production of short-chain fatty acids, collectively supporting gut and bone health. Additionally, Zn glycine mitigated LPS-induced oxidative stress by enhancing antioxidant enzyme activities and total antioxidant capacity while reducing oxidative damage markers. Importantly, Zn glycine preserved bone microarchitecture, increased (p < 0.01) bone mineral density (BMD), suppressed osteoclastic genes such as tumor necrosis factor receptor-associated factor 6 (TRAF6) and nuclear factor of activated T-cells cytoplasmic 1 (NFATC1), and promoted osteoblast activity through upregulation of runt-related transcription factor 2 (RUNX2), osteocalcin (OCN), and alkaline phosphatase (ALP). Mechanistically, these protective effects were mediated through inhibition of the TLR4/NF-κB signaling pathway. Overall, Zn glycine emerges as a promising nutritional strategy for preventing inflammation-driven bone loss via modulation of the gut-bone axis.

Ecotoxicology and Environmental SafetyVol. 309
South China Agricultural University (CN), Henan Agricultural University (CN), University of Agriculture Faisalabad (PK), University of Arkansas at Fayetteville (US)
Zero hunger
Openalex Percentile: Top 3%
Bone Metabolism and Diseases
22.24
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