Neuroendocrine tumours (NETs) have a unique ability to produce and secrete a variety of biogen amines and peptide hormones. They arise from multipotential stem cells, which differentiate during tumorigenesis into specific cell lines. Some of these tumours are functional, producing characteristic clinical syndromes. We present a female patient incidentally discovered to have diffuse liver metastases of neuroendocrine tumour of unknown primary origin. She was free of symptoms at initial presentation, and pathohistological analysis after liver biopsy revealed the tumour to be well differentiated (Ki-67 4.5%) with somatostatin positive in more than 70% of tumour cells. Fasting glycemia was normal, but results of oral glucose tolerance test were in favor of diabetes. Thorough examination including the octreoscan did not reveal the site of primary tumour. Expression of somatostatin receptors was intensive in metastases. Three months later, she reported episodes of night sweats, tremulousness, tachycardia and amnesia. Hypoglycemia was recorded during first hour of fasting, with extremely high levels of insulin and C-peptide. Further imunohistological investigation of tumor bioptate revealed positivety for proinsulin in 30%, and insulin in less than 0.2% of tumour cells. After the initiation of diazoxide the glycemic control was improved but only after the initiation of combined therapy with short-acting somatostatin analogue she managed to have euglycemia during the whole day. In an attempt to control both endocrinological syndrome and tumour growth, the patient underwent hemoembolisation. Clinical syndromes caused by plurihormonal secretion make therapeutical treatment difficult, especially in cases of cosecretion of physiological antagonists.