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Leucine Kinetics and the Effects of Hyperinsulinemia in Patients With Cushing’s Syndrome^*

Cattedra di Malattie del Ricambio, Istituto di Medicina Clinica, and Semeiotica Medica (G.M., F.M.), University of Padova Padova, Italy

Address all correspondence and requests for reprints to: Paolo Tessari, M.D., Cattedra di Malattie del Ricambio, Policlinico Universitario, Via Giustiniani, 2 35128 Padova, Italy.

As muscle wasting and resistance to insulinmediated glucose utilization are features of Cushing’s syndrome (CS), we examined glucose and amino acid metabolism in six patients with CS and six normal subjects before and during euglycemic hyperinsulinemic clamp studies (plasma insulin concentrations, 0.36, 0.65, and 10.05 mmol/L). The two groups had similar body mass index values. In the postabsorptive state, leucine and a-ketoisocaproate (KIC) rates of appearance (Ra), KIC oxidation, and nonoxidized leucine-carbon flux, an index of leucine entering protein (LeuP), were comparable in CS patients [2.38 ± 0.14 (±SE), 0.22 ± 0.04, and 2.16 ± 0.12 µmol/kg·min) and in normal subjects (2.73 ± 0.25, 0.17 ± 0.02, and 2.59 ± 0.22 /unol/kg·min). During the euglycemic clamp studies the leucine and KIC Ra values, KIC oxidation, and LeuP decreased to a similar extent in both groups. In contrast, insulinmediated glucose utilization was impaired in the CS patients at each clamp step (P < 0.05). In summary, postabsorptive whole body leucine metabolism is normal in patients with CS and is normally suppressed by hyperinsulinemia, indicating a dissociation in insulin sensitivity with respect to glucose and amino acid metabolism.

^* Presented in part at the 12th Congress of the International Diabetes Federation, Madrid, Spain, September 23–28,1985, Supported by a grant from the National Research Council (CNR) of Italy (No. 870024304).

Received July 7, 1987.

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