ArticleBMC biology2020
PHOSPHO1 is a skeletal regulator of insulin resistance and obesity.
Article in BMC biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Bone as an endocrine regulator of lipid and energy metabolism.Reviews in endocrine & metabolic disorders · 2026Review
- Genomic Insights Into Carnivorous Fish in the Characiformes.Ecology and evolution · 2026Article
- Panx3 deficiency in mice impairs bone fracture healing and causes transient hypoglycemia in neonatal animals.Molecular medicine (Cambridge, Mass.) · 2026Article
- Modulating Galectin-1 in human osteoblast-like cells alters mineralisation and influences the expression of genes associated with osteoblasts and osteocytes.Bioscience reports · 2026Article
- The role of bone in whole-body energy metabolism.Nature reviews. Endocrinology · 2025Review
- Distinct bone metabolic networks identified inFrontiers in medicine · 2025Article
- gNR4Aly Link Bridging Cellular Metabolism, Lactylation, and Vascular Calcification.Circulation research · 2024Article
- Bone mineralisation and glucose metabolism.Current opinion in endocrine and metabolic research · 2023Review
- Effects of DNA methylation on cardiometabolic risk factors: a systematic review and meta-analysis.Archives of public health = Archives belges de sante publique · 2022Review
- PiT2 deficiency prevents increase of bone marrow adipose tissue during skeletal maturation but not in OVX-induced osteoporosis.Frontiers in endocrinology · 2022Article
- The emerging roles of PHOSPHO1 and its regulated phospholipid homeostasis in metabolic disorders.Frontiers in physiology · 2022Review
- MicroRNA-29a in Osteoblasts Represses High-Fat Diet-Mediated Osteoporosis and Body Adiposis through Targeting Leptin.International journal of molecular sciences · 2021Article
- A 6-CpG validated methylation risk score model for metabolic syndrome: The HyperGEN and GOLDN studies.PloS one · 2021Article
Corrections and comments
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Authors and funding
20 authors at 10 institutions in 4 countries.
Funding
Abstract
backgroundThe classical functions of the skeleton encompass locomotion, protection and mineral homeostasis. However, cell-specific gene deletions in the mouse and human genetic studies have identified the skeleton as a key endocrine regulator of metabolism. The bone-specific phosphatase, Phosphatase, Orphan 1 (PHOSPHO1), which is indispensable for bone mineralisation, has been recently implicated in the regulation of energy metabolism in humans, but its role in systemic metabolism remains unclear. Here, we probe the mechanism underlying metabolic regulation by analysing Phospho1 mutant mice.
resultsPhospho1
conclusionWe show that mice lacking the bone mineralisation enzyme PHOSPHO1 exhibit improved basal glucose homeostasis and resist high-fat-diet-induced weight gain and diabetes. This study identifies PHOSPHO1 as a potential bone-derived therapeutic target for the treatment of obesity and diabetes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.