Fig. 9. Proposed hypotheses regarding the pathophysiology of gyrate atrophy. (1, hyperornithinemia hypothesis; 2, phosphocreatine deficiency hypothesis; 3, Δ1-pyrroline-5-carboxylate/proline deficiency hypothesis; 4, decarboxylation product excess (putrescine and other polyamines) hypothesis; OAT, ornithine aminotransferase; –, negative inhibition; ↑ , increase; ↓ , decrease)