Augmentation of protein degradation by l-triiodothyronine in uremia

Abstract

To ascertain if excessive protein catabolism is a feature of uremia, we determined leucine flux and nitrogen balance in 11 stable chronic dialysis patients and in 7 normal subjects. Leucine flux was determined during primed constant infusion of 2H 3 and 15N leucine. Nitrogen balance was determined by measurement of nitrogen in the food, dialysate, and urine, and in the dialysis patients by correcting for the changing urea nitrogen pool. To assess if thyroid hormone adversely affects protein metabolism, the above-mentioned studies were done once in the basal state and once after a 7-day course of l-triiodothyronine (T 3) treatment. Leucine carbon flux (μmol/kg/min) was 1.22 ± 0.05 in the controls and 1.40 ± 0.09 in the renal patients in the basal state ( P = NS). Following T 3 treatment, leucine carbon flux was increased to 1.40 ± 0.05 and 1.72 ± 0.09, respectively, in the controls and the renal patients ( P < .05). Fractional increment of the leucine carbon flux was 14% ± 3% in the controls and 23% ± 9% in the renal patients ( P < .05). The leucine nitrogen flux (μmol/kg/min) was 2.10 ± 0.15 in the controls and 2.54 ± 0.23 in the renal patients in the basal state ( P = NS), and increased to 2.48 ± 0.14 and 3.44 ± 0.22, respectively, in controls and renal patients after T 3 administration ( P < .05). Fractional increment of leucine nitrogen flux was 19.5% ± 4.3% in the controls and 36.4% ± 5.0% in the renal patients ( P < .05). During T 3 treatment, nitrogen output increased by 5% in the controls and by 16.4% in the renal patients ( P < .001). These data are consistent with a greater proteolytic response to thyroid hormone in dialysis patients.