This discrepancy between the animal and the human studies may be because the apoA-I levels in the animal studies were increased with infusions of unmodified, lipid-free apoA-I, whereas the analyses in the human study were based entirely on differences in endogenous plasma levels of apoA-I that is likely to have undergone post-translational modification and varying amounts of inactivation depending on the duration of the gestational diabetes [50,83]. This evidence concerns the gene APOA1 and gestational diabetes.