Kvetny J, Matzen L
Department of Clinical Chemistry, Odense University Hospital, Denmark.
J Endocrinol. 1990 Mar;124(3):495-9. doi: 10.1677/joe.0.1240495.
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 less than 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 less than 0.05) in patients with NTI (10.1 +/- 3.0 fmol/100 micrograms DNA) compared with controls (2.5 +/- 0.9 fmol/100 micrograms DNA). Unstimulated glucose uptake was increased in cells from patients with NTI (2.03 +/- 0.49 mmol/l per mg DNA per h, P less than 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 less than 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 less than 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.
对非甲状腺疾病(NTI)患者的单核血细胞进行了核三碘甲状腺原氨酸(T3)结合以及甲状腺激素刺激的耗氧量和葡萄糖摄取检测。与健康对照受试者(1.45±0.30 nmol/l)相比,NTI患者血清T3显著降低(P<0.05)(0.62±0.12(标准差)nmol/l)。患者血清促甲状腺激素(TSH)和性激素结合球蛋白与对照组均无差异。与对照组(2.5±0.9 fmol/100μg DNA)相比,NTI患者的核T3结合能力增强(P<0.05)(10.1±3.0 fmol/100μg DNA)。与对照组(1.13±0.20 mmol/l每毫克DNA每小时)相比,NTI患者细胞的基础葡萄糖摄取增加(2.03±0.49 mmol/l每毫克DNA每小时,P<0.01)。与对照组(0.26±0.12 mmol/l每毫克DNA每小时)相比,NTI患者细胞甲状腺素刺激的葡萄糖摄取(刺激后的葡萄糖摄取-基础葡萄糖摄取)增加(2.06±1.67 mmol/l每毫克DNA每小时,P<0.01),并且NTI患者细胞T3刺激的葡萄糖摄取也增加(1.34±0.81 mmol/l每毫克DNA每小时,P<0.05)。相比之下,基础耗氧量和甲状腺激素刺激的耗氧量均无差异。我们得出结论,核T3结合增加以及甲状腺激素诱导的葡萄糖摄取增加可能均代表倾向于维持细胞内稳态的反调节机制。