The stimulation of sugar transport in heart cells grown in a serum-free medium by picomolar concentrations of thyroid hormones: the effects of insulin and hydrocortisone.

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.