To define the biochemistry of tumor hypoglycemia, the metabolism of glucose and lactate were investigated in a patient with hypoglycemia associated with an adrenocortical carcinoma. Glucose and lactate kinetics and interconversion were determined by a primed-infusion technic in which 100 μc. each of glucose-1 and L-(+) lactate-U-C-14 were administered over a four-hour period on successive days before and after removal of the tumor. Before removal of the tumor, 400 gm. of glucose per day were required to maintain normoglycemia. Glucose turnover and its conversion to lactate were increased to values that were two to three times those observed in five normal subjects studied by these technics. Glucose oxidation and its contribution to the fuel of respiration were also enhanced. Although all aspects of glucose metabolism were quantitatively increased, no single route of glucose disposal was responsible for the accelerated turnover, and the pattern of metabolism was qualitatively normal. Despite excessive cortisol production, endogenous glucose production was paradoxically suppressed to 20 per cent of normal, and lactate incorporation into glucose was inhibited. Plasma free fatty acid concentrations were normal but did not respond to the administration of epinephrine. Following surgery, the hypoglycemia disappeared, glucose and lactate turnover returned to normal, and gluconeogenesis from lactate increased. Immunoreactive insulin and insulin-like activity in the plasma were not increased and extracts of the tumor did not produce hypoglycemia when injected into mice.

The hypoglycemia in this patient was due to a combination of increased glucose utilization and decreased glucose production. The data are consistent with the concept that these tumors synthesize and release a substance, which is currently unidentified, which acts on peripheral tissues and liver in a manner similar to insulin but which is undetectable by immuno- and bioassay technics.

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