Chronic acetyl-L-carnitine alters brain energy metabolism and increases noradrenaline and serotonin content in healthy mice

Smeland, Olav B., Meisingset, Tore W., Borges, Karin and Sonnewald, Ursula (2012) Chronic acetyl-L-carnitine alters brain energy metabolism and increases noradrenaline and serotonin content in healthy mice. Neurochemistry International, 61 1: 100-107. doi:10.1016/j.neuint.2012.04.008


Author Smeland, Olav B.
Meisingset, Tore W.
Borges, Karin
Sonnewald, Ursula
Title Chronic acetyl-L-carnitine alters brain energy metabolism and increases noradrenaline and serotonin content in healthy mice
Journal name Neurochemistry International   Check publisher's open access policy
ISSN 0197-0186
1872-9754
Publication date 2012-07
Sub-type Article (original research)
DOI 10.1016/j.neuint.2012.04.008
Volume 61
Issue 1
Start page 100
End page 107
Total pages 8
Place of publication Oxford, United Kingdom
Publisher Elsevier
Collection year 2013
Language eng
Formatted abstract
Acetyl-L-carnitine (ALCAR), the short-chain ester of carnitine, is a common dietary supplement readily
available in health food stores, claimed to improve energy levels and muscle strength. ALCAR has numerous
effects on brain and muscle metabolism, protects against neurotoxic insults and may be an effective
treatment for certain forms of depression. However, little is known about the effect of chronic ALCAR supplementation
on the brain metabolism of healthy mice. Here, we investigated ALCAR’s effect on cerebral
energy and neurotransmitter metabolism after supplementing the drinking water of mice with ALCAR for
25 days, providing a daily dose of about 0.5 g/kg. Thereafter the animals were injected with [1-13C]glucose,
and 13C incorporation into and levels of various metabolites were quantified in extracts of the hippocampal
formation (HF) and cortex using 1H- and 13C-nuclear magnetic resonance (NMR) spectroscopy
and high performance liquid chromatography (HPLC). Increased glucose levels were detected in both
regions together with a decreased amount of [3-13C]lactate, but no alterations in incorporation of 13C
derived from [1-13C]glucose into the amino acids glutamate, GABA and glutamine. These findings are consistent
with decreased metabolism of glucose to lactate but not via the TCA cycle. Higher amounts of the
sum of adenosine nucleotides, phosphocreatine and the phosphocreatine/creatine ratio found in the cortex
of ALCAR-treated mice are indicative of increased energy levels. Furthermore, ALCAR supplementation
increased the levels of the neurotransmitters noradrenaline in the HF and serotonin in cortex,
consistent with ALCAR’s potential efficacy for depressive symptoms. Other ALCAR-induced changes
observed included reduced amounts of GABA in the HF and increased myo-inositol. In conclusion, chronic
ALCAR supplementation decreased glucose metabolism to lactate, resulted in increased energy metabolite
and altered monoamine neurotransmitter levels in the mouse brain.
Keyword Metabolomics
Glucose
Phosphocreatine
Adenosine nucleotide
Monoamines
NMR spectroscopy
Alcar
Depression
Food supplement
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2013 Collection
School of Biomedical Sciences Publications
 
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