Insulin clamp studies were carried out in 50 individuals, 25 with normal glucose tolerance and 25 with non-insulin-dependent diabetes mellitus (NIDDM). Both diagnostic groups were further subdivided on the basis of body mass index (BMI) into an obese (BMI greater than 28 kg/m2) or nonobese group (BMI less than 28 kg/m2). The obese and nonobese subjects in each diagnostic category had similar plasma glucose levels in response to an oral glucose challenge. In addition, insulin-stimulated glucose utilization, as assessed by determination of glucose metabolic clearance rate (MCR), was not different as a function of obesity. Glucose MCR (mean +/- SEM) in obese subjects (mean BMI = 32.1) with normal glucose tolerance was 162 ml/min/m2, as compared with a value of 205 ml/min/m2 in nonobese individuals (mean BMI = 23.8). This difference was not statistically significant. Similarly, glucose MCR in obese patients (mean BMI = 34.7) with NIDDM was 55 ml/min/m2, as compared with a value of 80 ml/min/m2 in nonobese subjects (mean BMI = 24.9) with NIDDM. However, as can be seen from the above data, glucose MCR in patients with NIDDM, either nonobese or obese, was markedly reduced (P less than 0.001) when compared with that of normal subjects. These data emphasize the profound effect of NIDDM on reducing in vivo insulin action, and point out that the impact of obesity on insulin resistance is minor in comparison.
Glucose disposal rates (Rd) during an insulin clamp study reflect both basal and insulin-stimulated Rd. To quantify the amount of glucose taken up in response to a known increase in insulin concentration, two consecutive studies were performed on 10 patients with mild to moderate NIDDM (mean fasting glucose = 146 mg/dl) and 10 normal subjects. Endogenous insulin secretion was inhibited by somatostatin and plasma glucose level maintained at 180 mg/dl for 5. Rd (mg/m2/min) was determined isotopically for 2.5 h at insulin concentrations approximately 6 microU/ml and during 2.5 h of physiologic hyperinsulinemia at approximately 60 microU/ml (total glucose disposal), with the increase in Rd resulting from the approximate 10-fold elevation of plasma insulin concentration defined as insulin-stimulated glucose disposal. Results showed that the increment in Rd resulting from the elevation of plasma insulin concentration was relatively minor in NIDDM (38 +/- 6), increasing from a mean (+/- SEM) value of 83 +/- 8 to 121 +/- 12. Similar values in normal subjects were 90 +/- 7 and 274 +/- 26 with an increment of 183 +/- 21. Thus, insulin-stimulated glucose uptake in patients with NIDDM was only one-fifth of that in normals, and accounted for only 31% (38 divided by 121) of total glucose disposal during the clamp study. These data indicate that the majority of previous insulin clamp studies of in vivo insulin action in patients with NIDDM, in which total glucose disposal and insulin-stimulated glucose disposal have been equated, have underestimated the magnitude of insulin resistance present in NIDDM.(ABSTRACT TRUNCATED AT 250 WORDS)
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