ALTERATIONS OF SERUM CONCENTRATIONS OF THYROID-HORMONES AND SEX HORMONE-BINDING GLOBULIN, NUCLEAR-BINDING OF TRI-IODOTHYRONINE AND THYROID HORMONE-STIMULATED CELLULAR UPTAKE OF OXYGEN AND GLUCOSE IN MONONUCLEAR BLOOD-CELLS FROM PATIENTS WITH NONTHYROIDAL ILLNESS

Nuclear tri-iodothyronine (T3) binding and thyroid hormone-stimulated oxygen consumption and glucose uptake were examined in mononuclear blood cells from patients with non-thyroidal illness (NTI) in which serum T3 was significantly (P < 0.05) depressed (0.62 ± 0.12 (S.D.) nmol/l) compared with healthy control subjects (1.45 ± 0.30 nmol/l). Neither serum TSH nor sex hormone-binding globulin differed from that of the control group. Nuclear T3 binding capacity was increased (P < 0.05) in patients with NTI (10.1 ± 3.0 fmol/100 μg DNA) compared with controls (2.5 ± 0.9 fmol/100 μg DNA). Unstimulated glucose uptake was increased in cells from patients with NTI (2.03 ± 0.49 mmol/l per mg DNA per h, P < 0.01) compared with controls (1.13 ± 0.20 mmol/l per mg DNA per h). Thyroxine-stimulated glucose uptake (stimulated glucose uptake - unstimulated glucose uptake) was increased in cells from patients with NTI (2.06 ± 1.67 mmol/l per mg DNA per h, P < 0.01) compared with controls (0.26 ± 0.12 mmol/l per mg DNA per h), and T3-stimulated glucose uptake was also increased in cells from patients with NTI (1.34 ± 0.81 mmol/l per mg DNA per h, P < 0.05) compared with controls (0.24 ± 0.10 mmol/l per mg DNA per h). In contrast, neither unstimulated nor thyroid hormone-stimulated oxygen consumption differed. We conclude that both increased nuclear T3 binding and increased thyroid hormone-induced glucose uptake may represent counter-regulatory mechanisms which tend to maintain intracellular homeostasis.