The alpha2L111R,N122D isoform of the Na,K-ATPase expressed in HeLa cells does not undergo an adipocyte-like increase in activity in response to insulin.

In the rat adipocyte, insulin increases potassium uptake by a preferential activation of the alpha2 isoform of the Na,K-ATPase. The question under consideration here is whether expression of the alpha2 isoform is sufficient to replicate its differential activation by insulin. Accordingly, we compared the effect of insulin on the activity of the ouabain resistant rat alpha1 and alpha2RD (alpha2L111R,N122D) isoforms in HeLa cells. In HeLa cells, in contrast to the rat adipocyte, insulin produces an increase of equal magnitude in the rate of 86Rb+/K+ uptake by the ouabain resistant rat alpha1 and rat alpha2RD subunits. We conclude that the mechanism of insulin activation of the alpha2RD isoform in HeLa cells differs from that of the wild type alpha2 isoform in the rat adipocyte.