The effects of somatostatin on hormonal and metabolic responses in chronic pancreatitis

Unmodified synthetic somatostatin, given as a 200-μg intravenous bolus, plus 200 μg infused over 3 hours, had no effect on basal plasma insulin and pancreatic glucagonlike immunoreactivity (GLI) levels, both in controls and in patients with chronic pancreatitis. Somatostatin inhibited insulin-hypoglycaemia-induced pancreatic GLI release in controls and in patients with pancreatitis, and prolonged the insulin-induced fall in blood glucose in the patients. Arginine, presumably via insulin release, caused a fall in free fatty acids (FFA) in controls, which was inhibited by somatostatin. Somatostatin abolished the rebound rise in plasma FFA in patients with pancreatitis after insulin-hypoglycaemia. This effect may be related to inhibition of pancreatic GLI release or may be a direct action of somatostatin on lipolysis.