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자료유형
학술저널
저자정보
Megan C. Moorer (Johns Hopkins University School of Medicine) Ryan C. Riddle (Johns Hopkins University School of Medicine)
저널정보
대한내분비학회 Endocrinology and Metabolism Endocrinology and Metabolism Vol.33 No.3
발행연도
2018.1
수록면
318 - 330 (13page)

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Wnt/β-catenin signaling plays a critical role in the achievement of peak bone mass, affecting the commitment of mesenchymal progenitorsto the osteoblast lineage and the anabolic capacity of osteoblasts depositing bone matrix. Recent studies suggest that thisevolutionarily-conserved, developmental pathway exerts its anabolic effects in part by coordinating osteoblast activity with intermediarymetabolism. These findings are compatible with the cloning of the gene encoding the low-density lipoprotein related receptor-5(LRP5) Wnt co-receptor from a diabetes-susceptibility locus and the now well-established linkage between Wnt signaling and metabolism. In this article, we provide an overview of the role of Wnt signaling in whole-body metabolism and review the literature regardingthe impact of Wnt signaling on the osteoblast’s utilization of three different energy sources: fatty acids, glucose, and glutamine. Special attention is devoted to the net effect of nutrient utilization and the mode of regulation by Wnt signaling. Mechanisticstudies indicate that the utilization of each substrate is governed by a unique mechanism of control with β-catenin-dependent signalingregulating fatty acid β-oxidation, while glucose and glutamine utilization are β-catenin-independent and downstream of mammaliantarget of rapamycin complex 2 (mTORC2) and mammalian target of rapamycin complex 1 (mTORC1) activation, respectively. The emergence of these data has provided a new context for the mechanisms by which Wnt signaling influences bone development.

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