Article

Postprandial metabolism of meal triglyceride in humans

Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Biochimica et Biophysica Acta (Impact Factor: 4.66). 05/2012; 1821(5):721-6. DOI: 10.1016/j.bbalip.2012.01.006
Source: PubMed

ABSTRACT The intake of dietary fat above energy needs has contributed to the growing rates of obesity worldwide. The concept of disease development occurring in the fed state now has much support and dysregulation of substrate flux may occur due to poor handling of dietary fat in the immediate postprandial period. The present paper will review recent observations implicating cephalic phase events in the control of enterocyte lipid transport, the impact of varying the composition of meals on subsequent fat metabolism, and the means by which dietary lipid carried in chylomicrons can lead to elevated postprandial non-esterified fatty acid concentrations. This discussion is followed by an evaluation of the data on quantitative meal fat oxidation at the whole body level and an examination of dietary fat clearance to peripheral tissues - with particular attention paid to skeletal muscle and liver given the role of ectopic lipid deposition in insulin resistance. Estimates derived from data of dietary-TG clearance show good agreement with clearance to the liver equaling 8-12% of meal fat in lean subjects and this number appears higher (10-16%) in subjects with diabetes and fatty liver disease. Finally, we discuss new methods with which to study dietary fatty acid partitioning in vivo. Future research is needed to include a more comprehensive understanding of 1) the potential for differential oxidation of saturated versus unsaturated fatty acids which might lead to meaningful energy deficit and whether this parameter varies based on insulin sensitivity, 2) whether compartmentalization exists for diet-derived fatty acids within tissues vs. intracellular pools, and 3) the role of reduced peripheral fatty acid clearance in the development of fatty liver disease. Further advancements in the quantitation of dietary fat absorption and disposal will be central to the development of therapies designed to treat diet-induced obesity. This article is part of a Special Issue entitled Triglyceride Metabolism and Disease.

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    • "However, difference in the ability to incorporate NEFA could cause the different NEFA levels between the control and active FM periods; thus we consider that the control FM period might less incorporate NEFA than the active FM period. Such NEFA which is not incorporated and remaining in the bloodstream is known to be crucial for the late postprandial rise in NEFA [23,24]. "
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    • "In addition, incretin-mediated changes in portal insulin and glucagon concentrations may have masked effects of oral lipid ingestion on liver glucose metabolism, which is sensitive to small changes in portal insulin and glucagon (30). Incretins can also increase lipoprotein lipase activity in adipose tissue (31), thereby further increasing the release and uptake of FA from chylomicrons and reducing the spillover (i.e., the release into the blood) (32), which is in line with the observation of elevated chylomicrons, but not FA, in the current study. "
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    • "Another possible explanation relates to the TAG reservoirs that are known to exist in enterocytes [19]. It might be that the lipids of the DPA breakfast were stored in the enterocytes and released either over a longer time span than the 5 h that were followed in this study or after the following meal. "
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