FIG. 5.
Diagrammatic representation of the current hypothesis for changes in cerebral metabolic rates for glucose (CMRglc) after injury and ketosis among postnatal day 35 (PND35) and PND70 rats. The normal glucose metabolic pathway is shown for both sham PND35 and PND70 standard-fed rats (A). Both PND35 and PND70 rats show similar decreases in CMRglc after controlled cortical impact (CCI) on standard diet. Increased glucose processing through the pentose phosphate pathway has only been determined in the PND70 age group (B). Injured PND35 animals maintained on the ketogenic (KG) diet showed a further decrease in CMRglc, which may be directly related to greater ketone metabolism, which contributes more to the acetylCoA pool and consequently inhibits pyruvate oxidation (C). It remains unclear at this time whether there is a threshold of pyruvate oxidation inhibition that alters glucose uptake. PND70 rats on the KG diet showed normalization of the CMRglc rates (D). In this case, while ketones are likely to be metabolized, there are normal rates of glucose uptake, which may be subsequently shunted to other pathways. It is hypothesized that the increased activities in alternative metabolic pathways may contribute to this glucose uptake and may result in detrimental byproducts after traumatic brain injury.