Müller M J, Acheson K J, Jequier E, Burger A G
Medizinische Hochschule Hannover, Universität Hannover, Federal Republic of Germany.
Am J Physiol. 1988 Aug;255(2 Pt 1):E146-52. doi: 10.1152/ajpendo.1988.255.2.E146.
The glucoregulatory function of thyroid hormones was investigated in six healthy subjects before and after 14 day 3,5,3',5'-tetraiodothyronine (T4) treatment (300 micrograms/day) using a sequential clamp protocol for 5 h at euglycemia (0-2 h) and hyperglycemia (165 mg/dl, 2-5 h) and different insulin infusion rates (1.0 for 0-3.5 h and 6.5 mU.kg-1.min-1, for 3.5-5 h). T4 treatment increased basal energy expenditure (+8%), glucose disposal (+31%), and oxidation (+87%) but decreased nonoxidative glucose metabolism (-30%) and was without effect on lipid oxidation. During the euglycemic clamp, T4 treatment enhanced insulin-induced glucose disposal (+16%), glucose oxidation (+34%), and inhibition of lipid oxidation (-66 vs. -40%); nonoxidative glucose metabolism was stimulated to a similar extent before and after T4. During hyperglycemia, 3,5,3'-triiodothyronine (T3) did not affect glucose disposal but increased carbohydrate-induced lipogenesis at both insulin infusion rates. We conclude that T4 treatment promotes glucose disposal and oxidation, T3 decreases noninsulin-mediated glucose storage but does not antagonize insulin action.
采用序贯钳夹方案，在6名健康受试者接受14天3,5,3',5'-四碘甲状腺原氨酸（T4）治疗（300微克/天）前后，于正常血糖（0 - 2小时）和高血糖（165毫克/分升，2 - 5小时）状态下，以不同胰岛素输注速率（0 - 3.5小时为1.0，3.5 - 5小时为6.5微单位·千克⁻¹·分钟⁻¹）持续钳夹5小时，研究甲状腺激素的葡萄糖调节功能。T4治疗使基础能量消耗增加（+8%）、葡萄糖处置增加（+31%）以及氧化增加（+87%），但非氧化葡萄糖代谢减少（-30%），且对脂质氧化无影响。在正常血糖钳夹期间，T4治疗增强了胰岛素诱导的葡萄糖处置（+16%）、葡萄糖氧化（+34%）以及对脂质氧化的抑制（-66对-40%）；T4治疗前后非氧化葡萄糖代谢受到的刺激程度相似。在高血糖期间，3,5,3'-三碘甲状腺原氨酸（T3）不影响葡萄糖处置，但在两种胰岛素输注速率下均增加了碳水化合物诱导的脂肪生成。我们得出结论，T4治疗促进葡萄糖处置和氧化，T3减少非胰岛素介导的葡萄糖储存，但不拮抗胰岛素作用。
