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 ± 0·1 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.
Journal of Endocrinology (1990) 124, 495–499
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