The anti-somatostatin agents used to treat acromegaly, Cushing's disease and neuroendocrine tumours also have hyperglycaemic effects. This is particularly true for pasireotide. Hyperglycaemic events are seen in 57–73% of patients with Cushing's treated with pasireotide, with a need to initiate antidiabetic treatment in about 50% of these patients. In acromegaly, treatment with pasireotide induces hyperglycaemia in 29–61% of patients. Pasireotide-induced hyperglycemia occurs early, within the first 3 months of treatment, due to a decrease in insulin secretion secondary to a fall in secretion of GLP-1 and GIP, and potentially also due to a direct inhibitory effect of pasireotide on beta cells. Close monitoring of blood glucose is mandatory in all patients during the first 3 months of treatment with pasireotide. Where necessary, antidiabetic treatment should be initiated, preferably with a DPP-4 inhibitor or a GLP-1 receptor agonist, both of which have proven efficacy in the control of hyperglycaemia induced by pasireotide.