Insulin resistance implies that the body's cells (primarily muscle) lose sensitivity to insulin, a hormone secreted by the pancreas to promote glucose utilization. At the molecular level, a cell senses insulin through insulin receptors, with the signal propagating through a cascade of molecules collectively known as PI3K/Akt/mTOR signaling pathway.[8] Recent studies suggested that the pathway may operate as a bistable switch under physiologic conditions for certain types of cells, and insulin response may well be a threshold phenomenon.[2][8][9] The pathway's sensitivity to insulin may be blunted by many factors such as free fatty acids, causing insulin resistance. From a broader perspective, however, sensitivity tuning (including sensitivity reduction) is a common practice for an organism to adapt to the changing environment or metabolic conditions.[10] Pregnancy, for example, is a prominent change of metabolic conditions, under which the mother has to reduce her muscles' insulin sensitivity to spare more glucose for the brains (the mother's brain and the fetal brain). This can be achieved through raising the response threshold (i.e., postponing the onset of sensitivity) by secreting placental growth factor to interfere with the interaction between insulin receptor substrate (IRS) and PI3K, which is the essence of the so-called adjustable threshold hypothesis of insulin resistance