Background: The intestinal peptide transporter PEPT-1 plays an important role in development, growth, reproduction and stress tolerance in C. elegans as revealed by the severe phenotype of the pept-1-deficient strain pept-1. The reduced number of offspring and increased stress resistance were shown to result from changes in the insulin/IGF-signaling cascade. To further elucidate the regulatory network behind the phenotypic alterations in PEPT1-deficient animals a quantitative proteome analysis combined with transcriptome profiling was applied. Results: Various target genes of XBP-1, the major mediator of the unfolded protein response, were found to be down-regulated at mRNA and protein level, accompanied by a reduction of spliced xbp-1 mRNA. Proteome analysis also revealed a markedly reduced content of numerous ribosomal proteins. This was associated with a reduction in the protein synthesis rate in pept-1 C. elegans, a process that is strictly regulated by the TOR (target of rapamycine) complex, the cellular sensor for free amino acids. Conclusion: These data argue for a central role of PEPT-1 in cellular amino acid homeostasis. In PEPT-1 deficiency, amino acid levels dropped down systematically leading to alterations in protein synthesis and in the IRE-1/XBP-1 pathway.