ArticleNature communications2024
Targeting osteoblastic 11β-HSD1 to combat high-fat diet-induced bone loss and obesity.
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Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed.
- Recent advances in glucocorticoid regulation of bone and the bone marrow niche: Genetic and pharmacological approaches to understand and prevent bone loss.Current opinion in endocrine and metabolic research · 2026Article
- Renaissance of Traditional Mineral Drugs in Cancer: Advanced Delivery Strategies and Bioengineering Approaches.Pharmaceutics · 2026Review
- Myostatin Research: From Molecular Understanding to Clinical Translation for Musculoskeletal and Metabolic Disorders.International journal of molecular sciences · 2026Review
- Programmed PTH pulsatility coupled with piezoelectric stimulation via ultrasound-activated scaffolds synergizes deep bone defect regeneration.Bioactive materials · 2026Article
- Adipocytic sclerostin loop3-LRP4 interaction required by sclerostin to impair whole-body lipid and glucose metabolism.Nature communications · 2026Article
- New therapeutic target for osteoarthritis: modulating immune-metabolic aberrations and micromilieu remodeling in underlying bone.Frontiers in pharmacology · 2026Review
- Context-dependent roles of 11β-HSD1 in bone and skeletal muscle diseases.American journal of translational research · 2026Review
- The roles, mechanisms, and therapeutic implications of glucocorticoids in glucose and lipid metabolism.Military Medical Research · 2026Review
- Alternative methods for pharmacological research on the action mechanisms of natural products used in the treatment of type 2 diabetes: a systematic review.Frontiers in pharmacology · 2026Review
- Biomimetic Nanoparticles for Bone Regeneration: Construction Strategies and Therapeutic Mechanisms.International journal of nanomedicine · 2026Review
- Quantitative LFQ-DIA proteomics reveals FTH1-MCM5/WNT axis mediated osteoblastic dysfunction via ferroptosis drives diabetic osteoporosis.Scientific reports · 2025Article
- 11β-HSD1 inhibitor alleviates lipid metabolism disorder by activating the AMPK signaling pathway.Scientific reports · 2025Article
- High-fat diet, intestinal microecology and bone loss.Nutrition & metabolism · 2025Review
- Gut Microbiota Modulates Obesity-Associated Skeletal Deterioration Through Macrophage Aging and Grancalcin Secretion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Obesity: pathophysiology and therapeutic interventions.Molecular biomedicine · 2025Review
- Metabolic Dysfunction in Idiopathic Intracranial Hypertension: Current Theories and Updates.Aging and disease · 2024Review
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Authors and funding
42 authors.
Chuanxin Zhong *Law Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Nanxi Li *Law Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Shengzheng Wang *Department of Medicinal Chemistry, School of Pharmacy, Fourth Military Medical University, Xi'an, Shaanxi, China.
Dijie LiLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Zhihua YangThe Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.ORCID 0000-0002-9301-0317
Lin DuSports Medicine Center, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Guangxin HuangDepartment of Joint Surgery, The Third Affiliated Hospital of Southern Medical University, The Third School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Haitian LiLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Wing Sze YeungLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Shan HeDepartment of Materials Science and Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, China.
Shuting MaLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Zhuqian WangLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Hewen JiangSchool of Chinese Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China.
Huarui ZhangSchool of Chinese Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China.
Zhanghao LiLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Xiaoxin WenLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Song XueDepartment of Sports Medicine and Rehabilitation, Peking University Shenzhen Hospital, Shenzhen, China.
Xiaohui TaoLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.ORCID 0000-0002-7464-5691
Haorui LiSports Medicine Center, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Duoli XieLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Yihao ZhangLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Zefeng ChenLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Junqin WangDepartment of Materials Science and Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, China.
Jianfeng YanDepartment of Materials Science and Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, China.
Zhengming LiangLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Zongkang ZhangSchool of Chinese Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China.ORCID 0000-0003-1646-7871
Zhigang ZhongSports Medicine Center, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Zeting WuInternational Medical Service Center, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Chao WanKey Laboratory of Regenerative Medicine, Ministry of Education, School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.
Chao LiangDepartment of Biology, Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0002-5617-3483
Luyao WangLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Sifan YuGuangdong-Hong Kong-Macao Greater Bay Area International Research Platform for Aptamer-based Translational Medicine and Drug Discovery, Hong Kong SAR, China.ORCID 0000-0003-1117-4199
Yuan MaLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Yuanyuan YuLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.ORCID 0000-0003-1276-5695
Fangfei LiLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Yang ChenKey Laboratory of Phytochemistry and Natural Medicines, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.
Baoting ZhangGuangdong-Hong Kong-Macao Greater Bay Area International Research Platform for Aptamer-based Translational Medicine and Drug Discovery, Hong Kong SAR, China.ORCID 0000-0003-1421-0212
Aiping LyuLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China. aipinglu@hkbu.edu.hk.ORCID 0000-0002-2303-0494
Fuzeng RenDepartment of Materials Science and Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, China. renfz@sustech.edu.cn.ORCID 0000-0002-9310-2174
Hong ZhouBone Research Program, ANZAC Research Institute, The University of Sydney, Sydney, Australia. h.zhou@sydney.edu.au.ORCID 0000-0001-5899-9660
Jin LiuLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China. liujin@hkbu.edu.hk.ORCID 0000-0001-6308-6719
Ge ZhangLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China. zhangge@hkbu.edu.hk.ORCID 0000-0002-7807-7695
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive glucocorticoid (GC) action is linked to various metabolic disorders. Recent findings suggest that disrupting skeletal GC signaling prevents bone loss and alleviates metabolic disorders in high-fat diet (HFD)-fed obese mice, underpinning the neglected contribution of skeletal GC action to obesity and related bone loss. Here, we show that the elevated expression of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), the enzyme driving local GC activation, and GC signaling in osteoblasts, are associated with bone loss and obesity in HFD-fed male mice. Osteoblast-specific 11β-HSD1 knockout male mice exhibit resistance to HFD-induced bone loss and metabolic disorders. Mechanistically, elevated 11β-HSD1 restrains glucose uptake and osteogenic activity in osteoblast. Pharmacologically inhibiting osteoblastic 11β-HSD1 by using bone-targeted 11β-HSD1 inhibitor markedly promotes bone formation, ameliorates glucose handling and mitigated obesity in HFD-fed male mice. Taken together, our study demonstrates that osteoblastic 11β-HSD1 directly contributes to HFD-induced bone loss, glucose handling impairment and obesity.
Indexed as
11-beta-Hydroxysteroid Dehydrogenase Type 1Diet, High-FatMice, Inbred C57BLMice, KnockoutObesityOsteoblastsAnimalsBone ResorptionGlucocorticoidsGlucoseHumansMaleMiceOsteogenesisSignal Transduction11-beta-Hydroxysteroid Dehydrogenase Type 1GlucocorticoidsGlucoseHsd11b1 protein, mouse
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