The existence of a possible functional relationship between increased Alx3 and Foxo1 levels in the context of abnormally elevated concentrations of glucose was further investigated in primary MEM cells. We argued that if glucose-induced ALX3 is responsible for the increased expression of Foxo1, it could be expected that in cells lacking ALX3, expression of Foxo1 would not occur in response to increased concentrations of glucose. In turn, this would lead to impaired glucose-dependent expression of genes encoding oxidative stress detoxifying enzymes. To test this hypothesis, primary MEM cells were prepared from Alx3-null or control wild type embryos from non-diabetic pregnancies.