“…Proposed mechanisms include excessive glucose utilization by the tumor, impaired hepatic glycogenolysis and gluconeogenesis as a result of tumorinduced hepatic destruction or inhibition of normal counterregulatory responses that prevent hypoglycemia, and secretion of an insulin-like molecule, specifically insulin-like growth factor-2 (IGF-2) that lowers the blood glucose concentration by enhancing glucose utilization by normal cells (Cryer and Polonsky, 1998). Serum insulin concentrations are typically undetectable or in the lower end of the reference range with non-betacell tumors, in contrast to the high-normal to increased serum insulin concentrations seen with hypoglycemia induced by a betacell tumor (Beaudry et al, 1995;Bagley et al, 1996;Bellah and Ginn, 1996). IGF-2 is structurally homologous to proinsulin, can bind to insulin receptors, and has direct insulin-like actions that result in hypoglycemia (de Groot et al, 2007).…”