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成骨细胞中Wnt7b的过表达可刺激骨形成，并减轻高脂饮食小鼠的肥胖。

Wnt7b overexpression in osteoblasts stimulates bone formation and reduces obesity in mice on a high-fat diet.

作者信息

Song Fangfang, Marmo Tyler, Song Chao, Liao Xueyang, Long Fanxin

机构信息

State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, Hubei 430079, China.

Translational Research Program in Pediatric Orthopedics, Department of Surgery, The Children's Hospital of Philadelphia, Philadelphia, PA 19104, United States.

出版信息

JBMR Plus. 2024 Sep 23;8(11):ziae122. doi: 10.1093/jbmrpl/ziae122. eCollection 2024 Nov.

DOI:10.1093/jbmrpl/ziae122
PMID:39434845
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11491285/
Abstract

Previous studies have shown that Wnt7b potently stimulates bone formation by promoting osteoblast differentiation and activity. As high-fat feeding leads to obesity and systemic metabolic dysregulation, here we investigate the potential benefit of Wnt7b overexpression in osteoblasts on both bone and whole-body metabolism in mice fed with a high-fat diet (HFD). Wnt7b overexpression elicited massive overgrowth of trabecular and cortical bone but seemed to ameliorate body fat accumulation in mice with prolonged HFD feeding. In addition, Wnt7b overexpression modestly improved glucose tolerance in male mice on HFD. Collectively, the results indicate that targeted overexpression of Wnt7b in osteoblasts not only stimulates bone formation but also improves certain aspects of global metabolism in overnourished mice.

摘要

先前的研究表明，Wnt7b通过促进成骨细胞分化和活性来有力地刺激骨形成。由于高脂喂养会导致肥胖和全身代谢失调，因此我们在此研究在高脂饮食（HFD）喂养的小鼠中，成骨细胞中Wnt7b过表达对骨骼和全身代谢的潜在益处。Wnt7b过表达引发了小梁骨和皮质骨的大量过度生长，但在长期高脂饮食喂养的小鼠中似乎改善了体脂积累。此外，Wnt7b过表达适度改善了高脂饮食雄性小鼠的葡萄糖耐量。总体而言，结果表明，成骨细胞中Wnt7b的靶向过表达不仅刺激骨形成，还改善了营养过剩小鼠整体代谢的某些方面。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ba/11491285/f8a7e0b8ab23/ziae122f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ba/11491285/aa8b398b72b0/ziae122f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ba/11491285/ac6bf325ea80/ziae122f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ba/11491285/d5a3a4780084/ziae122f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ba/11491285/c016dbc068cd/ziae122f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ba/11491285/6421f300f99d/ziae122f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ba/11491285/f8a7e0b8ab23/ziae122f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ba/11491285/aa8b398b72b0/ziae122f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ba/11491285/ac6bf325ea80/ziae122f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ba/11491285/d5a3a4780084/ziae122f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ba/11491285/c016dbc068cd/ziae122f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ba/11491285/6421f300f99d/ziae122f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ba/11491285/f8a7e0b8ab23/ziae122f6.jpg

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本文引用的文献

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JCI Insight. 2023 Dec 22;8(24):e174293. doi: 10.1172/jci.insight.174293.
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Roles of osteocytes in phosphate metabolism.成骨细胞在磷酸盐代谢中的作用。
Front Endocrinol (Lausanne). 2022 Jul 15;13:967774. doi: 10.3389/fendo.2022.967774. eCollection 2022.
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WNT7B overexpression rescues bone loss caused by glucocorticoids in mice.WNT7B过表达可挽救小鼠中由糖皮质激素引起的骨质流失。
FASEB J. 2021 Jul;35(7):e21683. doi: 10.1096/fj.202100151RR.
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Gain-of-Function Lrp5 Mutation Improves Bone Mass and Strength and Delays Hyperglycemia in a Mouse Model of Insulin-Deficient Diabetes.功能获得性 Lrp5 突变可改善骨量和骨强度，并延缓胰岛素缺乏型糖尿病小鼠的高血糖。
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Malic Enzyme Couples Mitochondria with Aerobic Glycolysis in Osteoblasts.苹果酸酶将成骨细胞中的线粒体与有氧糖酵解偶联。
Cell Rep. 2020 Sep 8;32(10):108108. doi: 10.1016/j.celrep.2020.108108.
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Osteocalcin is necessary for the alignment of apatite crystallites, but not glucose metabolism, testosterone synthesis, or muscle mass.骨钙素对于磷灰石晶体的排列是必要的，但对于葡萄糖代谢、睾丸激素合成或肌肉质量则不是必需的。
PLoS Genet. 2020 May 28;16(5):e1008586. doi: 10.1371/journal.pgen.1008586. eCollection 2020 May.
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An osteocalcin-deficient mouse strain without endocrine abnormalities.一种不具有内分泌异常的骨钙素缺陷型小鼠品系。
PLoS Genet. 2020 May 28;16(5):e1008361. doi: 10.1371/journal.pgen.1008361. eCollection 2020 May.
8
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9
Increased glycolysis mediates Wnt7b-induced bone formation.糖酵解增加介导 Wnt7b 诱导的骨形成。
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Vhl deletion in osteoblasts boosts cellular glycolysis and improves global glucose metabolism.成骨细胞中 Vhl 的缺失会促进细胞糖酵解，并改善整体葡萄糖代谢。
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