دورية أكاديمية
Effects of PTH on osteoblast bioenergetics in response to glucose.
| العنوان: | Effects of PTH on osteoblast bioenergetics in response to glucose. |
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| المؤلفون: | DeMambro VE; Center for Molecular Medicine, MaineHealth Institute for Research, Scarborough, ME, USA.; Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, ME, USA., Tian L; Center for Molecular Medicine, MaineHealth Institute for Research, Scarborough, ME, USA., Karthik V; Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, ME, USA., Rosen CJ; Center for Molecular Medicine, MaineHealth Institute for Research, Scarborough, ME, USA.; Tufts University School of Medicine, Tufts University, Boston, MA, USA.; Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, ME, USA., Guntur AR; Center for Molecular Medicine, MaineHealth Institute for Research, Scarborough, ME, USA.; Tufts University School of Medicine, Tufts University, Boston, MA, USA.; Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, ME, USA. |
| المصدر: | Bone reports [Bone Rep] 2023 Jul 24; Vol. 19, pp. 101705. Date of Electronic Publication: 2023 Jul 24 (Print Publication: 2023). |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Elsevier Inc Country of Publication: United States NLM ID: 101646176 Publication Model: eCollection Cited Medium: Print ISSN: 2352-1872 (Print) Linking ISSN: 23521872 NLM ISO Abbreviation: Bone Rep Subsets: PubMed not MEDLINE |
| أسماء مطبوعة: | Original Publication: [Philadelphia] : Elsevier Inc., [2015]- |
| مستخلص: | Parathyroid hormone acts through its receptor, PTHR1, expressed on osteoblasts, to control bone remodeling. Metabolic flexibility for energy generation has been demonstrated in several cell types dependent on substrate availability. Recent studies have identified a critical role for PTH in regulating glucose, fatty acid and amino acid metabolism thus stimulating both glycolysis and oxidative phosphorylation. Therefore, we postulated that PTH stimulates increased energetic output by osteoblasts either by increasing glycolysis or oxidative phosphorylation depending on substrate availability. To test this hypothesis, undifferentiated and differentiated MC3T3E1C4 calvarial pre-osteoblasts were treated with PTH to study osteoblast bioenergetics in the presence of exogenous glucose. Significant increases in glycolysis with acute ∼1 h PTH treatment with minimal effects on oxidative phosphorylation in undifferentiated MC3T3E1C4 in the presence of exogenous glucose were observed. In differentiated cells, the increased glycolysis observed with acute PTH was completely blocked by pretreatment with a Glut1 inhibitor (BAY-876) resulting in a compensatory increase in oxidative phosphorylation. We then tested the effect of PTH on the function of complexes I and II of the mitochondrial electron transport chain in the absence of glycolysis. Utilizing a novel cell plasma membrane permeability mitochondrial (PMP) assay, in combination with complex I and II specific substrates, slight but significant increases in basal and maximal oxygen consumption rates with 24 h PTH treatment in undifferentiated MC3T3E1C4 cells were noted. Taken together, our data demonstrate for the first time that PTH stimulates both increases in glycolysis and the function of the electron transport chain, particularly complexes I and II, during high energy demands in osteoblasts. Competing Interests: The authors declare that there is no conflict of interest. (© 2023 The Authors.) |
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| معلومات مُعتمدة: | U54 GM115516 United States GM NIGMS NIH HHS |
| فهرسة مساهمة: | Keywords: Agilent seahorse cellular flux analyzer; Glycolysis; PTH bioenergetics; Plasma Membrane Permeabilizer Assay |
| تواريخ الأحداث: | Date Created: 20230814 Latest Revision: 20240416 |
| رمز التحديث: | 20240416 |
| مُعرف محوري في PubMed: | PMC10412867 |
| DOI: | 10.1016/j.bonr.2023.101705 |
| PMID: | 37576927 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 2352-1872 |
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| DOI: | 10.1016/j.bonr.2023.101705 |