Postprandial metabolism of meal triglyceride in humans
Open accessAbstract
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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While approximately 80% of the rise in triglyceride levels after a fat-load meal is due to intestinally derived B48-containing lipoproteins, apoB100-containing VLDL account for most, approximately 80%, of the increase in particle number.
“While ∼80% of the rise in TG levels after a fat-load meal is due to intestinally derived B48-containing lipoproteins, apoB100-containing VLDL account for most (∼80%) of the increase in particle number”
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Self-citation
- Authors
- Lambert, J. E., & Parks, E. J.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Parks, Elizabeth J.
- ORCID
- Parks, Elizabeth J.
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
- Publisher
- Elsevier BV
- Published
- 2012-05
- Volume
- 1821
- Issue
- 5
- Pages
- 721-726
- ISSN
- 1388-1981 (ISSN-L)
- PMC
- PMC3588585
- OpenAlex
- W2108090841
- Cited by
- 182
- References
- 83
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 10 · 2023: 14 · 2022: 23 · 2021: 11 · 2020: 11 · 2019: 18 · 2018: 8 · 2017: 10 · 2016: 11 · 2015: 11 · 2014: 20 · 2013: 15 · 2012: 7
- FWCI
- 2.79
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (RL1DK081187)
- National Center for Research Resources (KL2RR024983, TL1RR024984)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Keywords
- dietary fat absorption, chylomicrons, free fatty acids, fatty acid oxidation, fatty acid partitioning, ectopic fat deposition, insulin resistance, hepatic steatosis, diabetes mellitus, diet-induced obesity, cephalic phase, meal composition
- MeSH terms
- Dietary Fats, Eating, Humans, Liver, Obesity, Triglycerides, Muscle, Skeletal, Postprandial Period, Enterocytes, Lipid Metabolism
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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