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Abstract

Insulin resistance can be said to exist “whenever normal concentrations of hormone produce a less than normal biological response”. 1 In the 1930s, Himsworth first differentiated patients with diabetes mellitus into “insulin sensitive” and “insulin insensitive” based on the ability of subcutaneous insulin administration to dispose of an oral glucose load. 2. He further suggested that this differentiation corresponded to the clinical presentation of diabetes: that of either young ketosis-prone insulin sensitive or middle aged, nonketotic, insulin insensitive patients. The former is now classified as type 1 diabetes mellitus with the latter “insulin insensitive” classified as type 2 diabetes mellitus. Upon the development of the radioimmunoassay technique in 1960, Yalow and Berson demonstrated that patients with the adult-onset form of diabetes had, on average, higher circulating insulin levels than nondiabetic subjects. 3 It was thus concluded that “the tissues of the maturity onset diabetic do not respond to insulin as well as the tissues of the nondiabetic subjects respond to insulin.”

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Courtney, C.H., Olefsky, J.M. (2007). Insulin Resistance. In: Mechanisms of Insulin Action. Springer, New York, NY. https://doi.org/10.1007/978-0-387-72204-7_10

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