ietary fat is digestion begins within the mouth and stomach by the action of salivary lipase, and is subsequently completed in the small intestine by the action of pancreatic lipase. This process is enhanced in the duodenum by the action of bile, which emulsifies the lipids and allows more efficient interaction of the lipase enzymes with the lipids in the aqueous gut environment. Following digestion, the monoglycerides and fatty acids migrate to the unstirred layer of the small intestine and are absorbed by diffusion and active transport. Within the enterocytes, the fatty acids and monoglycerides are reformed into triglycerides, and along with other lipids such as cholesterol, are packaged into chylomicrons. Absorption of chylomicrons occurs through diffusion into lacteals across the porous and gelatinous basolateral surface of the enterocytes before entering the circulation via the subclavian vein.
Therefore postprandially, triglyceride levels rise as the influx of lipids in chylomicrons starts to arrive in the venous and then the arterial blood. Lipoprotein lipase can act on these chylomicrons and this causes the release of free fatty acids which are then taken up into tissues. However, not all of the fatty acids enter tissues immediately, and this causes a rise in plasma fatty acids postprandially. An increased free fatty acid concentrations in plasma is thought to contribute to the disease process because excess free fatty acids are a possible cause of insulin resistance in skeletal muscle and the liver. Certainly some of these fatty acids are derived from endogenous synthesis of triglycerides through hepatic fructose metabolism in the liver. However, evidence suggests that adiposity may increase the contribution of dietary fat to postprandial free fatty acid concentrations.
For example, in one study radiolabelled triglycerides at levels of 0.4 or 0.7 g per kg bodyweight were fed to healthy male subjects and plasma levels of fatty acids derived from the radiolabelled triglycerides were measured postprandially. The results showed that the spill over of fatty acids was not significantly different following the higher fat meal compared to the lower fat meal, and that the triglyceride response in plasma was also not different between the two meals. However, the increase in free fatty acids seen after the high fat meal was inversely proportional to the degree of adiposity in the subjects. Therefore postprandial rises in free fatty acids are larger for those men with lower levels of body fat. This may suggest that men with a higher percentage body fat are able to sequester more of the fatty acids from the postprandial lipids in their larger subcutaneous fat reserves compared to thinner men.
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