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N., Mariadi, I

Metabolic dysfunction induced by TBI impairs the availability/utilization of cerebral glucose for aerobic ATP generation and promotes release of alternative substrates (i.e

administered BPC 157 (10mcg/kg or 10 ng/kg) orally, in drinking water (12 ml/rat/day) or intraperitoneally (once daily, first application 30 min following surgery to test its effects on short bowel syndrome in rats, observing the effectiveness of both forms of administration [24]