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Understanding the mechanism of traumatic brain injury-induced energy metabolism

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The average adult human brain represents approximately 2% of the total body weight, yet it accounts for nearly 20 % of all the energy consumed. Under physiological conditions, human brain function and activity relies upon glucose metabolism that is precisely regulated by intrinsic mechanisms which are ...

The average adult human brain represents approximately 2% of the total body weight, yet it accounts for nearly 20 % of all the energy consumed. Under physiological conditions, human brain function and activity relies upon glucose metabolism that is precisely regulated by intrinsic mechanisms which are severely disrupted following traumatic brain injury (TBI). Convincing evidence shows that transient increase in cerebral glucose uptake/metabolism and in lactate/pyruvate ratio during acute phase of TBI and prolonged hypoglycemia and decreased glucose metabolism in the chronic phase of TBI are associated with increased mortality and poor out come irrespective of initial TBI severity and brain lesion volume. The underlying mechanism remains unknown. The transient hyperglycemia could be the result of traumatic stress response, the result of increased energy demand and/or ATP depletion following TBI. TBI may induce massive neuronal firing and ionic gradient disruption across the neuronal cell membrane via mechanical force and ligand-gated ion channels that causes massive potassium release into the extracellular space. In order to reinstate the disrupted ionic balance and to remove demised cell debris, brain ATP could be depleted very rapidly due to over-activated high energy-demanding ATP-dependent pumping mechanisms. Meanwhile, efficient ATP production from mitochondrial oxidative phosphorylation of glucose could be severely impaired or completely stopped due to TBI-induced ischemia and/or direct mitochondria damage. Recent experimental data support a decoupling of glycolysis and the tricarboxylic acid cycle. Other factors including cerebral blood flow, hypoxia, cortical spreading depression, inflammation, microglia activation, glutamate–glutamine recycling and glutamate detoxification pathways may also be involved in TBI-induced energy metabolism. The main aim of this research topic will be focused on mechanisms involved in the TBI-induced hyperglycemia and hypoglycemia. We would be interested in manuscripts describing the novel and unconventional mechanisms of TBI-induced energy metabolism. A glimpse into various aspects of the metabolic pathways is welcome. Like any other metabolic disorders, both genetic and environmental factors could play an important role in individual metabolic response to TBI. This so far has not been well studied. One question to ask is whether and how pre-trauma metabolic profile can affect TBI-induced energy metabolism and the outcome. Could genetic background and pre-existing energy metabolic profile be used to predict patient’s metabolic profile energy response and outcome following TBI? Is the altered pattern of glucose metabolism brain specific or global in nature? Solutions of these would have practical values in designing individualized treatment strategy. Papers addressing these questions would be particularly appreciated.


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