The delivery of free fatty acids (FFAs) to the liver is thought to be an important factor in the synthesis and secretion of very low-density lipoprotein triglyceride, a major determinant of circulating triglyceride concentrations. However, previous studies have found no correlation between plasma FFAs and plasma triglycerides. Adipose tissue lipolysis is suppressed after meals, primarily due to augmented insulin secretion. Because of this phenomenon, free-living individuals have FFA concentrations that are decreased below postabsorptive levels for the majority of the 24-hour period. However, relatively little attention has been given to postprandial FFA metabolism and its potential contribution to hepatic triglyceride production. We measured nocturnal and postprandial palmitate concentration and rate of appearance (Ra) in normotriglyceridemic control subjects (N=11); nondiabetic dyslipidemic subjects (N=28) receiving n-3 fatty acids (3 g/d), niacin (3 g/d), the combination (3 g/d each) or placebo; and subjects with poorly controlled type 2 diabetes (N=32). An extremely sensitive and precise HPLC method was used so that the very low FFA concentrations that occur postprandially could be accurately quantified. Nocturnal and postprandial palmitate Ra (using area under the curve analysis) was higher in dyslipidemic and diabetic than in control subjects (nocturnal 8.0±1.1 and 3.9±0.2 vs 1.8±0.4 mmol•m-2•h-1; postprandial 2.4±0.3 and 3.0±0.3 vs 1.1±0.1 mmol•m-2•h-1, all P≤0.001). The relative postprandial abnormality in Ra was greater than the nocturnal abnormality in diabetic individuals (P≤0.05), but not in those with dyslipidemia. The postprandial palmitate concentration nadir was greater in diabetic and dyslipidemic subjects than in controls (35±3 and 23±3 vs 11±2 μmol/L, both P≤0.01), indicating impaired meal suppression of lipolysis. There was no correlation between fasting FFA concentrations and fasting triglycerides in any group. However, postprandial nadir palmitate concentrations correlated with fasting triglycerides in both control and dyslipidemic subjects, (R=0.639, P≤0.05 and R=0.654, P≤0.005 respectively). There was no correlation in diabetic individuals (R=0.009, P=NS). These results indicate that abnormalities in postprandial adipose tissue lipolysis make an inordinate contribution to around-the-clock FFA economy in insulin resistant states such as DM. They also suggest that postprandial FFA availability may be an important determinant of total hepatic FFA delivery for very low-density lipoprotein triglyceride synthesis.
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