ArticleBone reports2021
β-Catenin mediates glucose-dependent insulinotropic polypeptide increases in lysyl oxidase expression in osteoblasts.
Article in Bone reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Gut hormones and bone homeostasis: potential therapeutic implications.Nature reviews. Endocrinology · 2024Review
- Correlation of Matrisome-Associatted Gene Expressions with LOX Family Members in Astrocytomas Stratified by IDH Mutation Status.International journal of molecular sciences · 2022Article
- [Gly²]-GLP-2, But Not Glucagon or [D-Ala²]-GLP-1, Controls Collagen Crosslinking in Murine Osteoblast Cultures.Frontiers in endocrinology · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Osteoblast lysyl oxidase (LOX) is a strongly up-regulated mRNA and protein by the glucose-dependent insulinotropic polypeptide (GIP). LOX is critically required for collagen maturation, and was shown to be dramatically down-regulated in a mouse model of type 1 diabetes, consistent with known low collagen cross-linking and poor bone quality in diabetic bone disease in humans and in mouse models. GIP is a gastric hormone released by the gut upon consumption of nutrients, which then stimulates insulin release from β-cells in the pancreas. GIP is directly anabolic to osteoblasts and to bone, while gut-derived dopamine attenuates effects of GIP on osteoblast anabolic pathways, including LOX expression. GIP-stimulation of LOX expression was shown to be dependent on increased cAMP levels and protein kinase A activity, consistent with the fact that GIP receptors are G protein coupled receptors. Downstream signaling events resulting in increased LOX expression remain, however, unexplored. Here we provide evidence for β-catenin mediation of signaling from GIP to increase LOX expression. Moreover, we have identified a TCF/LEF element in the
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Registered trials
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 Socratic graph.