Acetyl-l-carnitine modulates glucose metabolism and stimulates glycogen synthesis in rat brain

Aureli, Tommaso; Cocco, Maria Enrica Di; Puccetti, Caterina; Ricciolini, Rita; Scalibastri, Maurizio; Miccheli, Alfredo; Manetti, Cesare; Conti, Filippo

doi:10.1016/s0006-8993(98)00319-9

Cited by 33 publications

(23 citation statements)

References 35 publications

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“…It might be suggested that reduced impulsivity depends to some extent on these NA and 5-HT changes. ALC may act by improving energy and phospholipid metabolisms (Aureli et al 1998), and may protect neuronal function by action at the mitochondrial level (Hagen et al 2002;Virmani et al 2002;Beal 2003). Being a donor of acetyl groups, ALC is classically reported to enhance acetylcholine release (Imperato et al 1989) and to facilitate the neuronal response to acetylcholine (Tempesta et al 1985).…”

Section: Discussionmentioning

confidence: 99%

“…Great effort is devoted to the identification of novel non-psychostimulant agents, and acetyl-L-carnitine (ALC) has been proposed as a possible alternative. ALC is an energy reservoir (Aureli et al 1998), which is converted through deacetylation to carnitine. The latter is a carrier of long-chain fatty acids, which are important for brain maturation and functioning (Salvati et al 2000).…”

Section: Introductionmentioning

confidence: 99%

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Acetyl-l-carnitine reduces impulsive behaviour in adolescent rats

et al. 2004

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The attention deficit/hyperactivity disorder (ADHD) can affect human infants and adolescents. One important feature of this disorder is behavioural impulsivity. This study assessed the ability of chronic acetyl-L-carnitine (ALC, saline or 100 mg/kg SC, plus 50 mg/kg orally) to reduce impulsivity in a validated animal model for ADHD. Food-restricted rats were tested during adolescence (postnatal days, pnd, 30-45) in operant chambers with two nose-poking holes, one delivering one food pellet immediately, and the other five pellets after a delay. Delay length was increased over days (from 0 to 80 s). Individual differences in the preference-delay curve emerged, with the identification of two distinct subpopulations, i.e. one with a nearly horizontal curve and another with a very steep ("impulsive") slope. The impulsivity profile was slightly but consistently reduced by chronic ALC administration. Consistent results were also obtained with methylphenidate (MPH, saline or 3 mg/kg IP twice daily). Impulsive rats exhibited a lower metabolite/serotonin (5HIAA/5HT) ratio in the medial frontal cortex (MFC) and lower noradrenaline (NA) levels in the MFC and cingulate cortex (CC) when compared with the other subgroup. The ALC treatment increased NA levels in the CC and the 5HIAA/5HT ratio in both CC and MFC. Present data suggest that ALC, a drug devoid of psychostimulant properties, may have some beneficial effects in the treatment of ADHD children.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Acetyl-l-carnitine reduces impulsive behaviour in adolescent rats

et al. 2004

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“…Aureli et al [125] showed that administration of ALCAR (100 mg/kg) by i.p. injection 20 minutes prior to injection of labeled glucose led to a reduction in the oxidation of [U- 14 C]glucose for energy and in the incorporation of 13 C into amino acids and tricarboxylic acid cycle intermediates, consistent with sparing of glucose by use of the acetyl CoA from ALCAR for energy in brain.…”

Section: Neuroprotection By Acetyl-l-carnitine (Alcar)mentioning

confidence: 99%

l-Carnitine and Acetyl-l-carnitine Roles and Neuroprotection in Developing Brain

2017

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L-Carnitine functions to transport long chain fatty acyl CoAs into the mitochondria for degradation by β-oxidation. Treatment with L-carnitine can ameliorate metabolic imbalance in many inborn errors of metabolism. In recent years there has been considerable interest in the therapeutic potential of L-carnitine and its acetylated derivative acetyl-L-carnitine (ALCAR) for neuroprotection in a number of disorders including hypoxia-ischemia, traumatic brain injury, Alzheimer’s disease and in conditions leading to central or peripheral nervous system injury. There is compelling evidence from preclinical studies that L-carnitine and ALCAR can improve energy status, decrease oxidative stress and prevent subsequent cell death in models of adult, neonatal and pediatric brain injury. ALCAR can provide an acetyl moiety that can be oxidized for energy, used as a precursor for acetylcholine, or incorporated into glutamate, glutamine and GABA, or into lipids for myelination and cell growth. Administration of ALCAR after brain injury in rat pups improved long-term functional outcomes, including memory. Additional studies are needed to better explore the potential of L-carnitine and ALCAR for protection of developing brain as there is an urgent need for therapies that can improve outcome after neonatal and pediatric brain injury.

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“…Aureli et al (1998Aureli et al ( , 2000 observed that acetylcarnitine treatment increased glycogen synthesis in the brain and that long-term acetyl-carnitine treatment normalised age-related disturbances in brain function. Acetyl-L L -carnitine significantly reversed age-associated decline in mitochondrial membrane potential and cardiolipin content, and improved ambulatory activity (Hagen et al, 1998).…”

Section: Therapeutic Use Of Short-chain Acyl-carnitine Estersmentioning

confidence: 99%