Despite systemic delivery of insulin, pancreas-kidney transplantation in patients with diabetes results in carbohydrate metabolism similar to that in nondiabetic subjects receiving the same immunosuppressive agents after kidney transplantation.

The isotope dilution technique has been extensively used to assess insulin action in humans. To determine if nonsteady state (NSS) has led to erroneous estimates of hepatic and extrahepatic insulin sensitivity, we measured glucose turnover in healthy subjects during infusion of insulin at rates of 0.25, 0.6, and 2.0 mU.kg-1.min-1. Turnover was calculated using Steele's traditional NSS equations [fixed-effective volume (pV) method] as well as with methods [radioactive infused glucose (hot-GINF) or variable pV] designed to minimize NSS error. In contrast to the fixed-pV method, both the hot-GINF and variable-pV methods indicated that several hours were required for suppression of hepatic glucose release at all insulin concentrations and that small increases in plasma insulin (approximately 100 pmol/l) had comparable effects on glucose disappearance and hepatic glucose release. Nevertheless, despite these differences, when turnover during the final hour of the insulin infusions was plotted vs. the prevailing insulin concentration, all three methods yielded similar insulin dose-response curves for suppression of hepatic glucose release. Thus despite previous errors in measurement of glucose turnover, the widely accepted belief that the human liver is exquisitely sensitive to small changes in insulin is correct.

OBJECTIVE: To investigate the in vivo effect of exercise training at high and low intensity on b-adrenergic stimulated fat metabolism in obese men at rest. METHOD: Twenty-three obese, healthy subjects were randomly divided in a low-intensity exercise training program (40% VO 2max , n 7), a high-intensity exercise training program (70% VO 2max ; n 8), or a non-exercising control group (n 8). The exercise training program lasted for 12 weeks with a training frequency of 3 times per week. Before and after the intervention body composition and maximal aerobic capacity were measured as well as fat metabolism at rest and during b-adrenergic stimulation by isoprenaline. For comparison, six lean subjects served as a control group. They participated in a low-intensity exercise training program and underwent the same measurements as the obese subjects. RESULTS: Relative fat oxidation decreased signi®cantly during infusion of an increasing dose of isoprenaline in the obese lowintensity and high-intensity exercise training groups as well as in the lean group (P`0.01). Exercise training failed to in¯uence the effect of b-adrenergic stimulation on relative fat oxidation in obese men at both intensities and in lean men. In addition, badrenergic-mediated lipolysis did not seem to be different after low intensity exercise training in lean and obese men. Lipolysis might be increased after high-intensity exercise training in obese men. CONCLUSION: Low-and high-intensity exercise training in obese men failed to affect b-adrenergic mediated relative fat oxidation in vivo. b-Adrenergic-mediated lipolysis might be increased in obese men after HI exercise training only. The effect of low-intensity exercise training on b-adrenergic-mediated fat metabolism was similar in lean and obese men.

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[3-3H]glucose is frequently used to measure glucose turnover in humans. If fructose 6-phosphate-fructose 1,6-diphosphate cycling (Fpc) is negligible in both liver and muscle, then [3-3H]- and [6-14C]glucose (corrected for Cori cycle activity) should provide equivalent measures of glucose turnover. In addition, if glycogenolysis is fully suppressed, then [14C]lactate specific activity should equal that of [6-14C]glucose from which it was derived, and oxidation of [6-14C]glucose, as measured by rate of generation of 14CO2, should equal total glucose oxidation (i.e., that derived from intra- and extracellular pools) as measured by indirect calorimetry. To address these questions, glucose turnover was measured simultaneously with [3-3H]- and [6-14C]glucose in the basal state and in presence of low (approximately 200 pM) and high (approximately 750 pM) insulin concentrations. Glucose turnover rates measured with [3-3H]- and [6-14C]glucose were equivalent at all insulin concentrations, indicating that Fpc had no detectable effect on measurement of glucose appearance. [14C]lactate specific activity was lower (P less than 0.01) than that of [6-14C]glucose in the basal state but not during either low- or high-dose insulin infusion, implying that all lactate was derived from extracellular glucose. On the other hand, glucose oxidation as measured by rate of generation of 14CO2 was lower (P less than 0.05) than glucose oxidation as measured by indirect calorimetry during both insulin infusions, implying either that suppression of glycogenolysis was not complete in all tissues or that one or both of these techniques do not accurately measure glucose oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)