Apparent insulin resistance due to abnormal enzymatic insulin degradation: a new mechanism for insulin resistance.
A 16-year-old girl presented with severe, prolonged insulin resistance. Insulin antibodies, initially thought to be responsible for the insulin resistance, were suppressed using monocomponent insulin and immunosuppressive 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 molecular weight to insulin. These products were of similar molecular weight to material obtained by incubating 125I insulin with protease. Trasylol significantly reduced the patient's insulin requirements and normalised 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. We propose abnormally rapid insulin degradation to be a new mechanism of resistance to insulin therapy.
D000293:Adolescent; D007611:Aprotinin / Q000627:therapeutic use; D002850:Chromatography, Gel; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000188:drug therapy / Q000201:enzymology*; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood / Q000627:therapeutic use; D007333:Insulin Resistance
D007328:Insulin; D007611:Aprotinin