Under this postulate, in insulin resistant states, low hypothalamic dopamine activity allows for (potentiates) 1) an altered beta cell response to external (e.g., autonomic) stimuli that facilitates hyperinsulinemia and increased GSIS, as previous studies indicate [15], that may include low paracrine beta cell dopamine activity and 2) neuroendocrine mechanisms (as described in this study) facilitating insulin resistance to thereby establish a coordinated and controlled steady state hyperinsulinemic, insulin resistant condition (as observed in seasonal animals in the wild). Here, INS is linked to Hyperinsulinemia.