Gordon A, Schwartz H, Gross J
Endocrinology. 1986 Jan;118(1):52-7. doi: 10.1210/endo-118-1-52.
Chick embryo heart cells were propagated in a defined serum-free medium. They formed a confluent, synchronously contracting monolayer that is not different from myocytes grown in serum containing media. The uptake of 2-deoxy-D-[1-3H]glucose in these cells was stimulated by exposure to physiological concentrations of T3 (1 pM) and T4 (10 pM). Actinomycin-D and puromycin did not block the stimulation of 2-deoxy-D-[1-3H]glucose uptake when given with T3 throughout a 6-h incubation period. Cells grown in the absence of both insulin and hydrocortisone were unresponsive to T3. Insulin at 200 nM restored the sensitivity of the cells to 0.1 pM T3. Addition of 10 nM hydrocortisone to the growth medium enhanced the effects of T3 synergistically. The T3-stimulated sugar uptake was completely blocked by 5 X 10(-6) M cytochalasin B, suggesting that T3 acts, like insulin, by the translocation of glucose transporters to the plasma membrane.
鸡胚心脏细胞在一种特定的无血清培养基中增殖。它们形成了一个汇合的、同步收缩的单层细胞，这与在含血清培养基中生长的心肌细胞并无差异。暴露于生理浓度的T3（1 pM）和T4（10 pM）可刺激这些细胞对2-脱氧-D-[1-³H]葡萄糖的摄取。在整个6小时的孵育期内，当与T3一起给予放线菌素-D和嘌呤霉素时，它们并未阻断对2-脱氧-D-[1-³H]葡萄糖摄取的刺激作用。在既无胰岛素又无氢化可的松的情况下生长的细胞对T3无反应。200 nM的胰岛素可恢复细胞对0.1 pM T3的敏感性。向生长培养基中添加10 nM的氢化可的松可协同增强T3的作用。T3刺激的糖摄取被5×10⁻⁶ M的细胞松弛素B完全阻断，这表明T3与胰岛素一样，通过将葡萄糖转运体转运到质膜而起作用。
