Abstract
In this review, the thesis is presented that maternal hyperglycemia produces an overnourished, fat fetus. If the fetus has a predisposition for type 2 diabetes, then the fat deposition in the fetus is predominantly in the fetal visceral cavity. Visceral fat deposition is the origin of insulin resistance. The fat fetus begins life with its pancreatic output of insulin compromised. Thus, the stage is set for developing type 2 diabetes in its lifetime. This review supports the hypothesis that normalization of maternal nutrition and fucose will decrease the risk of type 2 diabetes.