Receptors for Insulin are present on liver, adipose tissue and muscles. In addition, there are Insulin Receptors present in arcuate nucleus of hypothalamus, which influences anorexogenic neurons through IRS2 and PI-3K signaling. They also causes the inhibition of Food intake by increasing the expression of POMC, and cleaving its protein to alpha melanocortio stimulating hormone (αMSH). This is however the same response produced by the release of "LEPTIN" that act on anorexogenic neurons, and stop eating behavior - similarly as insulin by producing (αMSH).
My question is: why insulin goes to brain and produce this effect when their was Leptin available to do the same task? What is the significance of Insulin action here?