ArticleCommunications biology2024
The microbial metabolite imidazole propionate dysregulates bone homeostasis by inhibiting AMP-activated protein kinase (AMPK) signaling.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Bone aging: a paradigm of multiscale degeneration and targeted rejuvenation.Bone research · 2026Review
- Microbiome histidine competition mediates dietary control of systemic imidazole propionate.bioRxiv : the preprint server for biology · 2026Article
- Metformin as a Metabolic Reprogramming Interface in Host-Pathogen and Bone Microenvironment Crosstalk: A Dual-Target Strategy Against Antimicrobial Resistance and Osteoporotic Bone Loss.Antibiotics (Basel, Switzerland) · 2026Review
- Gut-bone axis crosstalk: Microbiota-driven immune-metabolic-neural networks in bone disorders and precision interventions.Journal of orthopaedic translation · 2026Review
- The Polyphenol-Microbiota Axis: Molecular Mechanisms, Metabolic Pathways, and Therapeutic Perspectives in Human Health.Journal of personalized medicine · 2026Review
- Impact of sleeve gastrectomy on bone metabolism in obese patients: from mechanisms to clinical prevention.Frontiers in medicine · 2026Review
- Toward a gut-AMPK axis: the microbiome and AMPK signaling in nutrition and healthy aging.Frontiers in physiology · 2026Review
- Imidazole propionate ameliorates lipid metabolism in adipocytes to attenuate high-fat diet-induced obesity via PPAR signaling pathway.Lipids in health and disease · 2025Article
- POs-Ca Drives Osteogenic Differentiation of Human Dental Pulp Stem Cells Via AMPK-Dependent Autophagy Activation and Reciprocal Calcium-Autophagy Crosstalk.Stem cells international · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
Microbial metabolites provide numerous benefits to the human body but can also contribute to diseases such as obesity, diabetes, cancer, and bone disorders. However, the role of imidazole propionate (ImP), a histidine-derived metabolite produced by the intestinal microbiome, in bone metabolism and the development of osteoporosis is still poorly understood. In this study, we investigated the role of ImP and its underlying mechanisms in regulating bone homeostasis. When ImP was administered to 8-week-old mice for 4 weeks, bone loss was observed, along with a decrease in alkaline phosphatase-positive osteoblast cells. Additionally, bone marrow stromal cells (BMSCs) isolated from ImP-treated mice exhibited reduced osteogenic potential. In BMSCs from control mice, ImP treatment inhibited BMP2-induced osteoblast differentiation while promoting adipocyte differentiation. However, ImP had no effect on RANKL-induced osteoclast differentiation or activity in bone marrow macrophages. Mechanistically, ImP treatment increased p38γ phosphorylation and decreased AMPK (T172) phosphorylation in BMSCs. Suppression of p38γ expression using si-p38γ reversed the inhibitory effects of ImP on osteoblast differentiation, with a concurrent increase in AMPK (T172) phosphorylation. Conversely, ImP stimulated adipocyte differentiation by decreasing AMPK (T172) phosphorylation. Treatment with the AMPK agonist metformin significantly reversed the inhibitory effects of ImP on osteoblast differentiation and the promotion of adipocyte differentiation, along with enhanced AMPK (T172) phosphorylation. These findings suggest that the microbial metabolite ImP may disrupt bone homeostasis by stimulating p38γ phosphorylation and inhibiting the AMPK pathway, presenting a potential therapeutic target for managing metabolic bone diseases.
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