Objectives: The present study examines the kinetic of plasma triacylglycerol (TAG) after sequential ingestion of lunch and dinner as well as the contribution of dietary fat ingested at lunch to subsequent post-dinner TAG composition.
Method: Six healthy subjects were included. After standardized breakfast (7: 30AM), 2 mixed meals with fat loads composed of 44 g olive oil (rich in oleic acid) at lunch (12PM) and 44 g sunflower oil (rich in linoleic acid) at dinner (7PM) were ingested. [1-13C] palmitate was added in lunch only. Plasma TAG and chylomicron-TAG (CMTAG) levels were measured sequentially after meals. [1-13C] palmitate enrichment and concentrations of oleic acid and linoleic acid were measured in all lipid fractions.
Result: Post-dinner plasma TAG peak was delayed as compared to lunch (3 hours vs 1 hour, p=0.002) whereas the magnitude of the postprandial peaks was not significantly different between lunch and dinner (2.4+/-0.3 vs 2.0+/-0.4 mmol/L, p=0.85). [1-13C] palmitate enrichment was maximal 5 hours after lunch in all lipid fractions and decreased slowly thereafter. After dinner ingestion, the rate of decline of [1-13C] palmitate enrichment plateaued during the first 60 minutes. Oleic acid increased slightly and immediately after dinner and remained the predominant fatty acid in all lipid fractions during the first hour after dinner. A delayed peak of plasma and CM-TAG was observed after dinner as compared to lunch without difference in the magnitude of peaks.
Conclusion: The contribution of dietary fat ingested at lunch to post-dinner lipemia is confirmed despite the relatively long lasting interval between the 2 meals (7 h) and the absence of any early peak of plasma TAG after dinner.
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http://dx.doi.org/10.1016/s1262-3636(07)70169-6 | DOI Listing |
Int J Mol Sci
January 2022
Department of Cancer Systems Imaging, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Peroxisome proliferator-activated receptor delta (PPARD) is a nuclear receptor known to play an essential role in regulation of cell metabolism, cell proliferation, inflammation, and tumorigenesis in normal and cancer cells. Recently, we found that a newly generated villin-PPARD mouse model, in which PPARD is overexpressed in villin-positive gastric progenitor cells, demonstrated spontaneous development of large, invasive gastric tumors as the mice aged. However, the role of PPARD in regulation of downstream metabolism in normal gastric and tumor cells is elusive.
View Article and Find Full Text PDFPLoS One
March 2016
Heart Failure Discovery Performance Unit, Metabolic Pathways and Cardiovascular Therapeutic Area, GlaxoSmithKline, King of Prussia, Pennsylvania, United States of America.
Previous studies have shown that glucagon-like peptide-1 (GLP-1) provides cardiovascular benefits independent of its role on peripheral glycemic control. However, the precise mechanism(s) by which GLP-1 treatment renders cardioprotection during myocardial ischemia remain unresolved. Here we examined the role for GLP-1 treatment on glucose and fatty acid metabolism in normal and ischemic rat hearts following a 30 min ischemia and 24 h reperfusion injury, and in isolated cardiomyocytes (CM).
View Article and Find Full Text PDFAm J Clin Nutr
September 2013
Institut Pluridisciplinaire Hubert Curien, Centre National de la Recherche Scientifique UMR 7178, Université de Strasbourg, Strasbourg, France.
Br J Nutr
October 2009
Institute of Human Nutrition, Southampton General Hospital, UK.
Mechanisms underlying the lipodystrophy syndrome associated with antiretroviral therapy (ART) for HIV infection are not completely understood. We investigated the effect of ART on blood lipid concentrations in the fasting state and after consumption of a meal containing [1-13C]palmitic acid in HIV-positive men receiving nucleoside reverse transcriptase inhibitors (NRTI, n 7), NRTI combined with protease inhibitors (PI; NRTIPI, n 6), in HIV-positive but therapy-naïve men (noART, n 5) and in HIV-seronegative men (controls, n 6). HIV-positive subjects had higher fasting TAG concentrations and resting energy expenditure than controls.
View Article and Find Full Text PDFMol Cell Biochem
April 2008
Department of Biological Sciences, University of Hull, Cottingham Road, Kingston-upon-Hull HU6 7RX, UK.
Cardiac hypertrophy is an independent risk factor in the development of heart failure. However, the cellular mechanisms underlying the transition from compensated hypertrophy to heart failure are incompletely understood. The aim of this study was to investigate changes in myocardial substrate utilisation and function in pressure-overload hypertrophy (using 13C NMR spectroscopy) in parallel with alterations in the expression pattern of genes involved in cardiac fatty acid and glucose uptake and oxidation.
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