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Immediately following a fat-containing meal, plasma triglycerides rise over a period of hours, peaking at 4 hours and returning to baseline at 8 hours. This effect is more profound for CVD patientscontrols [ 6 ], an effect that may be due to slightly higher plasma triglyceride concentrations amongst the former. Postprandial lipemia is more profound and persistent when a saturated fat load replaces one of polyunsaturated fat [ 7 ]. Postprandial lipemia is also more profound and persistent when the fat load is consumed with alcohol [ 7 8 ]. Once again the enhancement of lipemia is more profound when polyunsaturated fat is replaced by saturated fat [ 7 ]. Comparison of the triglyceride fatty acid compositions of the fat load with those of the postprandial plasma showed them to be the same [ 9 ]. Thus, preprandial alcohol inhibits the lipolysis of the intestinally-derived lipoproteins, the chylomicrons. This is an interesting finding and when added to the observed effects of alcohol or acetate on adipose tissue lipolysis, indicates that alcohol ingestion inhibits both adipose tissue lipolysis and lipoprotein lipase (LPL). This is an unexpected finding given that adipose tissue lipolysis is inversely correlated with LPL activity; e.g., following a meal, increased LPL activity is associated with reduced adipose tissue lipolysis. On the basis of these observations, one can put forth the as yet untested hypothesis, “acetate inhibits LPL activity.” Given that household vinegar is dilute acetic acid, it is important to determine the effects of this common food ingredient on the metabolism of dietary fat.