These data: 1) quantify the extent to which the healthy liver manages its use of different sources of FAs that flow to it, 2) demonstrate how the postprandial reduction in adipose-NEFA flux may be partially replaced by other sources, and 3) highlight the potential for dietary FA spillover to support the continued dominance of NEFA as a substrate for VLDL-TG synthesis.

Dietary supplementation with omega-3 PUFA derived from fish, but not from vegetable sources, increased plasma adiponectin, suppressed inflammation, and prevented cardiac remodelling and dysfunction under pressure overload conditions.

Dietary supplementation with omega-3 PUFA attenuated pressure overload-induced LV dysfunction, which was associated with elevated plasma adiponectin.

The present study quantified dietary fatty acid flux in healthy men (n ‫؍‬ 6) who were fed a liquid formula through a duodenal feeding tube (continuous feeding group) or who consumed the same formula in meals (meal feeding group). A triacylglycerol (TAG) stable isotope was added to the formula to determine the entry of dietary fatty acids into the serum and its clearance to the liver and resecretion into serum via VLDL. The contribution of dietary fatty acids to serum nonesterified fatty acids (NEFAs) was higher with meal feeding (24.4 ؎ 2.6%) compared with continuous feeding (10.8 ؎ 2.9%, P < 0.01) and, when multiplied by the NEFA concentration, resulted in similar absolute fatty acid spillover. Diet-derived NEFAs subsequently represented 10.6 ؎ 1.2% and 4.7 ؎ 1.3% of hepatic VLDL-TAG (meal feeding vs. continuous feeding, respectively, P ‫؍‬ 0.004). Chylomicron remnant uptake by the liver contributed 9.3 ؎ 1.9% of fatty acids to hepatic VLDL-TAG synthesis with meal feeding compared with continuous feeding (4.4 ؎ 0.8%, P < 0.03). These data suggest that the extent of dietary fatty acid recycling via serum NEFAs and VLDL-TAG is determined by the rate of delivery of dietary fat to the intestine. The inefficient removal of dietary fat from the circulation may maintain VLDL-TAG production but may also result in prolonged postprandial lipemia. Diabetes 54:2668 -2673, 2005 E levated postprandial lipemia has been shown to correlate with increased cardiovascular disease risk (1). Triacylglycerols (TAGs) taken in from the diet are primarily stored in adipose and utilized for energy by peripheral tissues, but a portion of these fatty acids can clear to the liver. That the liver may coordinate its use of fatty acids that flow to it from many different sources (e.g., adipose, diet, etc.) provides an elegant example of physiology. However, in settings of expansion of adipose stores, or higher dietary fat intake, the liver's ability to handle alterations in fatty acid flux may be compromised. Studies in fasting individuals have shown that dysregulation of hepatic fatty acid usage of adipose-derived nonesterified fatty acids (NEFAs) contributes to impaired glucose tolerance (2), and an understanding of liver fatty acid partitioning during fasting and feeding will be necessary to formulate future dietary and therapeutic strategies for the treatment of elevated blood lipids in insulin resistance and diabetes. In a companion article (3) in this issue of Diabetes, we have described the use of multiple stable isotopes to quantitate the flux of fatty acids into the liver, where they are subsequently reassembled to TAGs, incorporated into VLDL particles, and secreted from the liver. In that article, fatty acids derived from adipose, lipogenesis, and diet were quantified in healthy men. Little is known about the role dietary fatty acid flux plays in liver lipid metabolism, and in the present analysis, we focused specifically on routes of dietary fatty acid entry into the serum and liver. To assess the influence of the rate of fatty ac...

Sources of fatty acids flowing to the liver may be used for triacylglycerol (TAG) synthesis. Our objective was to quantify contributions of nonesterified fatty acids (NEFAs), de novo lipogenesis, and dietary fatty acids to VLDL-TAG in the fed state after meal feeding in healthy subjects (n ‫؍‬ 6). The effect of substrate delivery rate was also determined by comparison with data obtained under a continuous-feeding regimen. A liquid diet was administered by mouth or via feeding tube. Contributions of NEFAs, de novo lipogenesis, and dietary fatty acids to VLDL-TAG were quantified using stable isotopes and gas chromatography-mass spectrometry.