In identifying physiological links between fat and ethanol, a variety of evidence leads us to focus on TG as a strong, positive correlate of ethanol and fat intake. Circulating TG rise in proportion to the amount of fat consumed (Bahceci et al., 1999; Schrezenmeir et al., 1997). TG also rise from alcohol consumption (Contaldo et al., 1989; Goude et al., 2002), and hypertriglyceridemia is known to be a strong indicator of alcoholism (Baraona et al., 1983). 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 led to the prediction that a high-fat meal and ethanol may interact in their stimulatory effect on TG levels in rats. Experiment 2 confirmed this prediction. Rats drinking ethanol after a HFD meal had markedly elevated levels of circulating TG compared to water-drinking rats after this HFD meal or ethanol-drinking rats after a LFD meal. The failure of ethanol, when combined with a LFD, high-carbohydrate meal, to raise TG levels compared to water alone
