Journal
STEM CELLS
Volume 33, Issue 7, Pages 2306-2319Publisher
WILEY
DOI: 10.1002/stem.2042
Keywords
Neural stem cell; Progenitor; Neurogenesis; Fatty acid oxidation; Proliferation; Differentiation
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Funding
- Newcastle University Centre for Brain Ageing and Vitality - (Biotechnology and Biological Sciences Research Council)
- Newcastle University Centre for Brain Ageing and Vitality - (Engineering and Physical Sciences Research Council)
- Newcastle University Centre for Brain Ageing and Vitality - (Economic and Social Research Council)
- Newcastle University Centre for Brain Ageing and Vitality - (Medical Research Council) [G0700718]
- UK NIHR Biomedical Research Centre in Age and Age Related Diseases award
- MRC Centre for Neuromuscular Disease Grant [G000608-1]
- Wellcome Trust Centre for Mitochondrial Research Grant [096919/Z/11/Z]
- DRC Cell Functional Analysis Core NIH Grant [DK17047]
- NIH [AG038305]
- MRC [G0700718] Funding Source: UKRI
- Medical Research Council [G0700718] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0510-10187] Funding Source: researchfish
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Neural activity is tightly coupled to energy consumption, particularly sugars such as glucose. However, we find that, unlike mature neurons and astrocytes, neural stem/progenitor cells (NSPCs) do not require glucose to sustain aerobic respiration. NSPCs within the adult subventricular zone (SVZ) express enzymes required for fatty acid oxidation and show sustained increases in oxygen consumption upon treatment with a polyunsaturated fatty acid. NSPCs also demonstrate sustained decreases in oxygen consumption upon treatment with etomoxir, an inhibitor of fatty acid oxidation. In addition, etomoxir decreases the proliferation of SVZ NSPCs without affecting cellular survival. Finally, higher levels of neurogenesis can be achieved in aged mice by ectopically expressing proliferator-activated receptor gamma coactivator 1 alpha (PGC1), a factor that increases cellular aerobic capacity by promoting mitochondrial biogenesis and metabolic gene transcription. Regulation of metabolic fuel availability could prove a powerful tool in promoting or limiting cellular proliferation in the central nervous system. Stem Cells 2015;33:2306-2319
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