Pancreatic beta cells secrete the proinsulin connecting peptide (C-peptide) and insulin on an equimolar basis. The C-peptide can thus be used as an indicator of endogenous insulin secretion in the presence of exogenously administered insulin. Using this approach, we have shown suppression of endogenous insulin release in healthy subjects during hypoglycemia induced by intravenous infusion of porcine insulin. Moreover, the suppression persists after the plasma glucose returns to fasting levels, suggesting that the recovery of beta cells from the effects of hypoglycemia is not immediate.

Factitious hyperinsulinism was suspected in a patient with an 11-year history of insulin-dependent, ketosis-prone diabetes mellitus who began to experience repetitive episodes of "spontaneous" hypoglycemia. Insulin mediation of the hypoglycemia was confirmed by documenting that urinary insulin and total extractable insulin in plasma increased during periods of hypoglycemia. Failure to detect significant amounts of human C-peptide by radioimmunoassay during periods of hypoglycemia or in response to stimulation with glucagon, leucine, or tolbutamide indicated that the insulin was not endogenous. The diagnosis of factitious hyperinsulinism was ultimately proved by the finding of radioactivity in the patient's urine after 131-I Hippuran was added to a vial of insulin found in the patient's room.

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