These contradictory results may in part be explained if insulin resistance was apparent in the kidneys of the db/db mice at the time point studied, which would plausibly increase FoxO1 activity, similar to the increased Igfbp-1 expression observed in rodent models of type 1 diabetes [46] which occurs due to an absence of insulin and insulin signalling. The gene discussed is IGFBP1; the disease is type 1 diabetes mellitus.