We analyzed the mitochondrion organelle in the long-lived daf-2 mutant to find out whether reduced insulin/IGF-1 signaling affects mitochondria and if so, whether these changes contributed to the longevity phenotype. Compared to wild-type C. elegans, the long-lived daf-2 mutant showed a better ability in maintaining a youthful mitochondrial morphology and respiratory function at an old age. We therefore asked whether a young daf-2 mutant worm is equipped with more young mitochondria (therefore, more healthy mitochondria) to withstand aging. However, on adult day 1 the total amount of mitochondrial proteins in a daf-2 mutant worm was found to be about the same as that in a wild-type worm. From quantitative proteomic analyses of purified mitochondria of wild type, daf-2 and daf-2; daf-16 mutant worms, we identified 81 up-regulated and 44 down-regulated mitochondrial proteins in the daf-2 mutant, and most of these changes were dependent on daf-16. These differentially expressed proteins revealed a shift of metabolic activity, especially in the metabolism of reactive oxygen species, branched-chain amino acids, β-alanine, propionate, and fatty acids. Further experiments suggested that altered metabolism contributed to the longevity of the daf-2 mutant. No abundance changes were detected in the electron transport chain proteins. There was a slight (10-20%) decrease of mitochondrial ribosomal proteins in the daf-2 mutant; although these changes were not significant for individual proteins, they were as a group. Consistently, by ribosome profiling, we found that the amount of assembled 28S mitochondrial ribosomes decreased by about 20% in the daf-2 mutant, suggesting a decrease in protein synthesis inside mitochondria and echoing with previously reported decrease of protein synthesis in the cytoplasm. We did not find evidence of mitonuclear protein imbalance in our data. Collectively, our results suggest that insulin/IGF-1 signaling regulates mitochondria and mitochondrial changes contribute to the longevity of the daf-2 mutant.