synthesize OX (Chang et al., 2004; Lo et al., 2007). Further investigations reveal a similar relationship of ethanol to OX. Studies in rats chronically consuming ethanol, which increases circulating TG (Chang et al., 2007a), demonstrate an analogous increase in OX in the PFLH (Lawrence et al., 2006). The involvement of OX in this positive relationship between fat and ethanol is also supported by injection studies, which show an increase in ethanol intake after hypothalamic OX injection (Schneider et al., 2007), increased intake of a HFD after ventricular OX injection (Clegg et al., 2002), and a reduction in ethanol craving and self-administration after peripheral administration of an OX 1 receptor antagonist (Lawrence et al., 2006). This evidence suggests that a positive feedback exists between OX and ethanol, similar to the relationship between OX and dietary fat.
