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. 2014 Sep 10;6(5):1759091414550997. doi: 10.1177/1759091414550997

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© The Author(s) 2014

This article is distributed under the terms of the Creative Commons Attribution 3.0 License (http://www.creativecommons.org/licenses/by/3.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (http://www.uk.sagepub.com/aboutus/openaccess.htm).

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Figure 1. — Fatty acid oxidation and ketogenesis by neurons and astroglia.

(a) Fatty acid oxidation in neurons (filled bars) and astroglia (blank bars) as determined by quantifying the amount of ¹⁴CO₂ derived from [1-¹⁴C]palmitic acid ([¹⁴C]PAL). 5-Amino-1 -β-d-ribofuranosyl-imidazole-4-carboxamide (AICAR), an AMP-activated protein kinase (AMPK) activator, did not alter the oxidative metabolism. (b) Total ketone body production in neurons and astroglia as determined by collecting the acid-soluble fraction derived from [¹⁴C]PAL. AICAR enhanced astroglial KB production. (c) Production of acetoacetate (AA) from PAL in neurons and astroglia as determined using the cyclic thio-NADH method. (d) Production of β-hydroxybutyrate (BHB) from PAL in neurons and astroglia as determined using the cyclic thio-NADH method with palmitic acid (PAL) and l-carnitine (LC). Glucose (2 mmol/L) was included in all assay media. Both AA and BHB production in astroglia were enhanced by AICAR, while neuronal AA or BHB was not statistically significantly altered by AICAR. Values are the mean ± SD (n = 4 for a and b, n = 6 for c and d). n.s. = not significant. *p < .05; **p < .05; ***p < .001 (grouped t test).