Preeclampsia is a severe complication of human pregnancy and an insulin resistant state has been demonstrated in this multisystem disorder, although its bases remain unclear. Inositol phosphoglycans P-type belongs to a family of putative insulin mediators and was described to exert many insulin-like effects on lipid and glucose metabolism. A definite association between this molecule and preeclampsia was reported. The systemic inflammatory activation that occurs in preeclampsia as a consequence of the immunological dysfunction can exacerbate placental insulin resistance leading to an over-expression of P-IPG as a counterregulatory mechanism to insulin resistance. Besides, the lipidic form of P-IPG was reported to be similar to endotoxins, and may represent the link between insulin resistance, systemic inflammation and increased angiogenic factors. In this article we propose a new working theory on insulin resistance and preeclampsia.