Acute pancreatitis is characterised by the oxidative and nitrosative stress, but contribution of these mechanisms to the tissue damage and endocrine pancreas dysfunction has been insufficiently studied. This study aimed to investigate the role of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric-oxide synthetase (NOS), in development of oxidative-nitrosative stress and potentially disturbed glucoregulation in the clinical model of acute pancreatitis. Results reveal acute pancreatitis as a condition associated with a significant derrangement of glucoregulation and increased oxidative-nitrosative stress, as well as a disturbed ADMAregulated nitric oxide (NO) synthesis. Both hyperglycaemia and oxidative-nitrosative stress were identified as potential significant determinants of decreased ADMA-bioavailibility during acute pancreatitis, while glucose intolerance, found in 64% of patients 1 month after acute pancreatitis, was found to be directly associated with ADMA-level during acute phase of illness. Sofar unrecognized insufficient inhibition of NO-synthesis in acute pancreatitis contributes significantly to the endocrine pancreas damage and might be responsible for subsequent development of diabetes mellitus.