Creatine-Enhanced Diet Alters Levels of Lactate and Free Fatty Acids After Experimental Brain Injury

Abstract

Free fatty acids (FFA) and lactic acid are markers of secondary cellular injury following traumatic brain injury (TBI). We previously showed that animals fed a creatine (Cr)-enriched diet are afforded neuroprotection following TBI. To further characterize the neuroprotective Cr diet, we studied neurochemical changes in cortex and hippocampus following a moderate injury. Adult rats were fed either a control or Cr-supplemented diet (0.5%, 1%) for 2 weeks before TBI. At 30 min or 6 h after injury, tissue was processed for quantitative analysis of neurochemical changes. Both lactate and FFA were significantly increased in all tissues ipsilateral to the injury. Cr-fed animals had significantly lower levels, although the levels were elevated compared to sham controls. Animals fed a 1% Cr-diet were afforded greater neuroprotection than animals fed a 0.5% Cr diet. These results support the idea that a Cr-enriched diet can provide substantial neuroprotection in part by suppressing secondary brain injury.

The Human Serotonin 1A Receptor Expressed in Neuronal Cells: Toward a Native Environment for Neuronal Receptors

“…Increasing evidence has demonstrated that creatine affords neuroprotection (Wilken et al, 1998;Sullivan et al, 2000;Zhang et al, 2003;Scheff and Dhillon, 2004). The mechanisms implicated in creatine neuroprotection are controversial but they appear to depend on an increase in cellular phosphocreatine stores (Brustovetsky et al, 2001).…”

Combination Therapies for Traumatic Brain Injury: Retrospective Considerations

“…In contrast, creatine pretreatment was the only strategy that had a significantly beneficial cortical tissue sparing compared with injured animals on a standard diet, which duplicated our previously published monotherapy findings. 71,73 Further, the combination therapy did not improve tissue sparing over creatine monotherapy.…”

“…Impairments in mitochondrial ATP biosynthesis seen after TBI can be partially offset by providing a diet high in creatine as a pre-treatment. 68,70 Indeed, dietary creatine supplementation as a mono-agent pre-injury treatment has been shown to afford significant neuroprotection in animal models of TBI [71][72][73] as well as other conditions such as Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and cerebral ischemia. Increased phosphocreatine availability and ATP synthesis, in conjunction with reduced mitochondrial impairment and improved calcium dynamics, are thought to contribute to the neuroprotective actions of creatine observed in these models.…”

A Potential Role for Creatine in Drug Abuse?

“…Moreover, creatine-treated rats displayed significantly increased mitochondrial membrane potentials, levels of mitochondrial calcium and ATP, and significantly decreased levels of reactive oxidative intermediaries, relative to rats not given creatine. In another work, rats fed a diet containing 1% creatine before experiencing controlled cortical contusions had significantly more sparing of cortical tissue and suppressed levels of lactate and free fatty acids than rats not given creatine [43]. Finally, creatine supplementation can also reduce (1) ischemia-mediated depletion of ATP and (2) caspace-3-activation and cytochrome c release, which are indicators of cell damage [44].…”