Abstract
Recently, several cases of short-chain acyl-CoA dehydrogenase (SCAD) deficiency (McKusick 201470) in humans have been described. Symptoms of this disorder are variable (Turnbull et al 1984; Amendt et al 1987; Coates et al 1988) and metabolic characteristics are not well understood. A mutant mouse (BALB/cBYJ) with no SCAD activity in liver, which is the first animal model of fatty acid oxidation disorders, has been reported (Wood et al 1989). To investigate the metabolic characteristics in these mice, we performed a series of experiments using liver perfusion techniques and HPLC
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