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PAOLO TESSARI, SANDRO INCHIOSTRO, GIANNI BIOLO, MARIA CRISTINA MARESCOTTI, GIUSEPPE FANTIN, MARIA TERESA BOSCARATO, GENNARO MEROLA, FRANCO MANTERO, ANTONIO TIENGO, Leucine Kinetics and the Effects of Hyperinsulinemia in Patients With Cushing’s Syndrome, The Journal of Clinical Endocrinology & Metabolism, Volume 68, Issue 2, 1 February 1989, Pages 256–262, https://doi.org/10.1210/jcem-68-2-256
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Abstract
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 (Leu→P), 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 Leu→P 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.
