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Presentation of a New Method for Specific Measurement of in Vivo Insulin-Stimulated Glucose Disposal in Humans: Comparison of This Approach with the Insulin Clamp and Minimal Model Techniques^*

Department of Medicine, Stanford University School of Medicine, and Geriatric Research, Education, and Clinical Center, Veterans Administration Medical Center, Palo Alto, California 94304

Address all correspondence and requests for reprints to: Gerald M. Reaven, M.D., Geriatric Research, Education, and Clinical Center, (640/182B), Veterans Administration Medical Center, 3801 Miranda Avenue, Palo Alto, California 94304.

This study was initiated to compare the abilities of two alternative approaches to the measurement of insulindependent glucose disposal in normal humans. The ability of insulin to stimulate glucose disposal was measured in 12 normal subjects by determining glucose disposal rates during insulin clamp studies carried out at both basal insulin concentrations (6 µU/ml) and during a period of sustained hyperinsulinemia (60 µU/ml). The increment in glucose disposal was defined as nsulin-dependent disposal and compared to estimates of insulin action generated by both the conventional insulin clamp approach and the minimal model technique. The results documented an extremely close correlation (r = 0.99; P 0.001) between the direct determination of insulin-dependent glucose disposal and insulin-stimulated glucose disposal as estimated by the insulin clamp technique. In contrast, there was a poor correlation (r = 0.44; P = NS) between insulin sensitivity as estimated by the minimal model technique and insulin-dependent glucose disposal. These results indicate that the value of lucose disposal determined by the insulin clamp approach, which includes both insulin-independent and insulin-dependent glucose disposal, provides an excellent estimate of insulin-dependent glucose disposal in subjects with normal glucose tolerance. Unfortunately, this does not appear to be true of the minimal model technique. However, it must be emphasized that these conclusions are only applicable to normal humans, and may not apply to normal subjects of other species or to humans under different physiological or pathological situations. {J Clin Endocrinol Metab 60: 723, 1985)

^* This work was supported by grants from the Research Service of the V.A., the NIH (RR-70-22, AM-30732, AM-07217, and AM-07148), and the Nora Eccles Treadwell Foundation.

Received August 28, 1984.

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