Apparent Insulin Resistance due to Abnormal Enzymatic Insulin Degradation: A New Mechanism for Insulin Resistance

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Abstract
A 16-yr-old [diabetic] girl presented with severe, prolonged insulin resistance. Insulin antibodies, initially thought to be responsible for the insulin resistance, were suppressed using monocomponent insulin and immunosuppresive therapy; however, insulin resistance persisted. Insulin kinetic studies suggested abnormal metabolism of a bolus injection of 125I insulin and the reappearance in the circulation of radioactive products, demonstrated by chromatography to be of different MW to insulin. These products were of similar MW to material obtained by incubating 125I insulin with protease. Trasylol significantly reduced the patient''s insulin requirements and normalized the disappearance of 125I insulin from the circulation. Prolonged treatment with Trasylol resulted in a fall in insulin requirement to non insulin-resistance levels. The insulin requirement remained static when Trasylol was ceased. Abnormally rapid insulin degradation may be a mechanism of resistance to insulin therapy.