Effect of 1α,25-dihydroxy vitamin D3 and vitamin E on insulin-induced glucose uptake in rat adipocytes

Vitamin E, an antioxidant, improves insulin sensitivity through the suppression of conventional PKC in vascular smooth muscle cells. It has been reported that vitamin E reduces platelet aggregation through the suppression of PKCα and β (Diabetes 47 (1998) 1494). On the other hand, 1α,25-dihydroxy vitamin D3 (1,25D3) activates conventional PKC and may subsequently cause insulin resistance. Against this background, we examined the effect of vitamin E and 1,25D3 on PKCβ and PKC ζ/λ activities in vitro and 10 nM insulin-induced glucose uptake in rat adipocytes. In vitro PKCβ activity of adipocytes was slightly decreased by the addition of 1 μM vitamin E, but not PKC ζ/λ activity. In contrast, a 10–1000 nM 1,25D3 dose responsively activated PKCβ activity of adipocytes (ED 50%, 10 nM), but not PKC ζ/λ activity. Pretreatment with 1 μM vitamin E for 60 min did not improve the insulin-induced glucose uptake. On the other hand, pretreatment with a 10–1000 nM 1,25D3 dose responsively suppressed insulin-induced glucose uptake. Moreover, 1,25D3 increased membrane-associated PKCβ immunoreactivity for 60 min, but no additional increase in membrane-associated PKCβ immunoreactivity during treatment with insulin was observed. These results suggest that 1,25D3 reduces insulin-induced glucose uptake via activation of PKCβ, but not vitamin E in rat adipocytes.