blood (Baraona et al., 1983; Siler et al., 1998) and a decrease in fat oxidation (Siler et al., 1998). This stimulatory effect of ethanol on circulating TG may contribute to the enhanced fat consumption seen in ethanol drinkers compared to non-drinkers in previous studies (Herbeth et al., 1988; Le Marchand et al., 1989; Männistö et al., 1997). This is supported by the finding that TG elevated by a high-fat meal are associated with an increase in caloric intake in a subsequent test meal (Gaysinskaya et al., 2007). Moreover, direct manipulations of TG levels reveal their importance in the control of food intake and body weight, as illustrated by the ability of fenofibrate, a TG-lowering drug, to prevent the development of obesity in mice fed a HFD (Jeong et al., 2004). In the clinical literature, ethanol consumed with a high-fat meal has been shown to exacerbate the lipemic effects of the dietary fat (Fielding et al., 2000; Pownall, 1994). This evidence supports the involvement of circulating TG in the positive relationship between ethanol and dietary fat.
