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Osteoclast precursors display dynamic metabolic shifts toward accelerated glucose metabolism at an early stage of RANKL-Stimulated osteoclast differentiation

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dc.contributor.authorKim, Jin-Man-
dc.contributor.authorJeong, Daewon-
dc.contributor.authorKang, Hyun Ki-
dc.contributor.authorJung, Sung Youn-
dc.contributor.authorMin, Byung-Moo-
dc.contributor.authorKang, Sam Sik-
dc.date.accessioned2013-01-14T08:48:26Z-
dc.date.available2013-01-14T08:48:26Z-
dc.date.issued2007-
dc.identifier.citationCELLULAR PHYSIOLOGY AND BIOCHEMISTRY; Vol.20, No.6, pp.935-946ko_KR
dc.identifier.issn1015-8987-
dc.identifier.urihttp://hdl.handle.net/10371/80512-
dc.description.abstractMature osteoclasts have an increased citric acid cycle and mitochondrial respiration to generate high ATP production and ultimately lead to bone resorption. However, changes in metabolic pathways during osteoclast differentiation have not been fully illustrated. We report that glycolysis and oxidative phosphorylation characterized by glucose and oxygen consumption as well as lactate production were increased during receptor activator of nuclear factor-kappa B ligand (RANKL)-induced osteoclastogenesis from RAW264.7 and bone marrow-derived macrophage cells. Cell proliferation and differentiation varied according to glucose concentrations (0 to 100 mM). Maximal cell growth occurred at 20 mM glucose concentration and differentiation occurred at 5 mM concentration. Despite the similar growth rates exhibited when cultured cells were exposed to either 5 mM or 40 mM glucose, their differentiation was markedly decreased in high glucose concentrations. This finding suggests the possibility that osteoclastogenesis could be regulated by changes in metabolic substrate concentrations. To further address the effect of metabolic shift on osteoclastogenesis, we exposed cultured cells to pyruvate, which is capable of promoting mitochondrial respiration. Treatment of pyruvate synergistically increased osteoclastogenesis through the activation of RANKL-stimulated signals (ERK and JNK). We also found that osteoclastogenesis was retarded by blocking ATP production with either the inhibitors of mitochondrial complexes, such as rotenone and antimycin A, or the inhibitor of ATP synthase, oligomycin. Taken together, these results indicate that glucose metabolism during osteoclast differentiation is accelerated and that a metabolic shift towards mitochondrial respiration allows high ATP production and induces enhanced osteoclast differentiation. Copyright (c) 2007 S. Karger AG, Basel.ko_KR
dc.language.isoenko_KR
dc.publisherKARGERko_KR
dc.subjectboneko_KR
dc.subjectmetabolic substrateko_KR
dc.subjectosteoporosisko_KR
dc.subjectosteoclastogenesisko_KR
dc.subjectmetabolic diseasesko_KR
dc.titleOsteoclast precursors display dynamic metabolic shifts toward accelerated glucose metabolism at an early stage of RANKL-Stimulated osteoclast differentiationko_KR
dc.typeArticleko_KR
dc.contributor.AlternativeAuthor김진만-
dc.contributor.AlternativeAuthor정대원-
dc.contributor.AlternativeAuthor강현기-
dc.contributor.AlternativeAuthor정성윤-
dc.contributor.AlternativeAuthor민병무-
dc.contributor.AlternativeAuthor강삼식-
dc.identifier.doi10.1159/000110454-
dc.citation.journaltitleCELLULAR PHYSIOLOGY AND BIOCHEMISTRY-
dc.description.tc12-
Appears in Collections:
College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
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