SF1 and Insulin resistance: Given that both SF-1 and POMC neurons are anatomical substrates for the actions of insulin [38, 51, 61], this ability of E2 to markedly attenuate inhibitory NOP receptor-mediated neurotransmission at every node comprising these anorexigenic VMN SF-1/ARC POMC synapses may represent a novel means of protection against the development of central insulin resistance.