2013
DOI: 10.1016/j.brainres.2013.08.044
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Glucose administration after traumatic brain injury improves cerebral metabolism and reduces secondary neuronal injury

Abstract: Clinical studies have indicated an association between acute hyperglycemia and poor outcomes in patients with traumatic brain injury (TBI), although optimal blood glucose levels needed to maximize outcomes for these patients’ remains under investigation. Previous results from experimental animal models suggest that post-TBI hyperglycemia may be harmful, neutral, or beneficial. The current studies determined the effects of single or multiple episodes of acute hyperglycemia on cerebral glucose metabolism and neu… Show more

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Cited by 34 publications
(39 citation statements)
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“…30 However, lactate and pyruvate can readily cross the blood-brain barrier and enter the tricarboxylic acid cycle, 31,32 being preferential oxidative energy substrates over glucose for neurons. 33,34 The beneficial effect of exogenous glucose, lactate, and pyruvate has been shown in some TBI models, [35][36][37] but these substrates only modestly reduce the lesion size, with no apparent functional protection in our model. However, when lactate or pyruvate is combined with LLL illumination, mitochondrial functions are improved either additively or synergistically, giving rise to a faster recovery and less brain tissue loss compared with LLL, pyruvate, or lactate alone.…”
Section: Discussionmentioning
confidence: 69%
“…30 However, lactate and pyruvate can readily cross the blood-brain barrier and enter the tricarboxylic acid cycle, 31,32 being preferential oxidative energy substrates over glucose for neurons. 33,34 The beneficial effect of exogenous glucose, lactate, and pyruvate has been shown in some TBI models, [35][36][37] but these substrates only modestly reduce the lesion size, with no apparent functional protection in our model. However, when lactate or pyruvate is combined with LLL illumination, mitochondrial functions are improved either additively or synergistically, giving rise to a faster recovery and less brain tissue loss compared with LLL, pyruvate, or lactate alone.…”
Section: Discussionmentioning
confidence: 69%
“…27,28 This has led investigators to theorize that endogenous levels of glucose may not be sufficient to meet increased energy consumption of the injured brain, which may result in a metabolic secondary injury. Moro et al 15 provide support for this hypothesis in a rodent model of controlled cortical impact where exogenous glucose initiated after injury provided significant cellular neuroprotection and improved cerebral metabolism. Likewise, Hill et al 14 examined the effects of persistent hyperglycemia as seen in diabetic patients, on animals that were treated with streptozotocin to induce Type 1 diabetes.…”
Section: Discussionmentioning
confidence: 87%
“…The multiple glucose injections also resulted in a significant prevention of cortical tissue loss at 15 days post-CCI. Because these doses of glucose increase blood glucose levels to between 17.0 and 19.5 mmol/L (Moro et al, 2013), the current results suggest that an acute period of hyperglycemia after experimental TBI may improve some neurological outcomes and, importantly, it exerts no detrimental effects in a rat model of TBI.…”
Section: Discussionmentioning
confidence: 80%
“…Lower doses of glucose (100 mg/kg) administered from 1–10 days after fluid percussion brain injury did not alter cognitive outcome 11–15 post-injury (Kokiko-Cochran et al, 2008). More recently, single or multiple injections of hyperglycemic doses of glucose within the first 6 hours after CCI injury were found to significantly attenuate TBI-induced reductions in CMRGlc and reduce neuronal injury in cortex and hippocampus at 24 h post-injury (Moro et al, 2013). …”
Section: Introductionmentioning
confidence: 99%
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