C/EBPb is a transcription factor involved in regulation of genes for the ornithine cycle, an enzyme system that is present in the liver and detoxifies ammonia produced by amino acid metabolism. We examined effects of starvation, which augments amino acid degradation leading to ammonia production, in C/EBP β-deficient mice. Starving the deficient mice for 48 h caused hyperammonemia. The starved C/EBP β-deficient mice exhibited also hypoglycemia, which apparently imposed degaradation of body protein to supply amino acids for gluconeogenesis and then imposed ammonia overproduction. Being concordant with this notion, more severe loss of body weight, liver weight and liver protein amount was observed in C/EBP β-deficient mice than in wild-type mice. On the other hand, mRNA and protein levels for the ornithine cycle enzymes in the liver under the starvation are roughly similar or rather up-regulated in C/EBP β-deficient mice compared to wild-type mice. Total protein amounts for the enzymes are comparable in starved mice of both genotypes, in spite of more severe loss of total liver protein in C/EBP β-deficient mice. Down-regulation of C/EBP α under starvation was relieved in C/EBP β-deficient mice, and induction of C/EBP δ augmented, both being apparently involved in compensating the lack of C/EBP β.