Abstract
THE first evidence for an abnormality in insulin receptor capacity in pathological states was provided by Kahn et al.1, who found that liver plasma membranes from the obese hyperglycaemic mouse bound only a fraction of insulin compared with membranes from lean littermates. A similar observation was made with lymphocytes from obese insulin-resistant diabetic patients2. In lymphocyte cultures the insulin concentration in the medium seemed to determine the binding capacity of the cells3. These results suggested an inverse relationship between the number of receptors and the surrounding concentration of insulin, regardless of the tissue sensitivity to the hormone. We have now found greater than normal binding capacity in the diabetic Chinese hamster, which has genetic insulin deficiency, in many ways resembling juvenile diabetes4.
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