It has been observed that such reductions in hypothalamic dopaminergic activity in insulin resistant states are coupled to elevations of noradrenergic and serotonergic activities at the ventromedial hypothalamus (VMH) and elevated Neuropeptide Y and corticotropin releasing hormone levels at the hypothalamic paraventricular nucleus (PVN), in which neurophysiological alterations have been shown to markedly potentiate insulin resistance in part via a concurrent loss of appropriate hypothalamic fuel sensing (as discussed above) and an elevation of sympathetic tone in the periphery [30–34, 46]. This evidence concerns the gene CRH and Insulin resistance.