Postprandial Lipid Response Following a High Fat Meal in Rats Adapted to Dietary Fiber

1992 ◽  
Vol 122 (2) ◽  
pp. 219-228 ◽  
Author(s):  
Carol L. Redard ◽  
Paul A. Davis ◽  
Suzette J. Middleton ◽  
Barbara O. Schneeman
Keyword(s):  
Dietary Fiber ◽  
High Fat ◽  
Lipid Response ◽  
Postprandial Lipid ◽  
Fat Meal

scholarly journals An exome-wide sequencing study of lipid response to high-fat meal and fenofibrate in Caucasians from the GOLDN cohort

2018 ◽  
Vol 59 (4) ◽  
pp. 722-729 ◽  
Author(s):  
Xin Geng ◽  
Marguerite R. Irvin ◽  
Bertha Hidalgo ◽  
Stella Aslibekyan ◽  
Vinodh Srinivasasainagendra ◽  
...  
Keyword(s):  
Rare Variants ◽  
Transcript Level ◽  
Lipid Lowering ◽  
Gene Transcript ◽  
High Fat ◽  
Heart Study ◽  
Lipid Response ◽  
Coding Variants ◽  
Fat Meal ◽  
Meal Challenge

Our understanding of genetic influences on the response of lipids to specific interventions is limited. In this study, we sought to elucidate effects of rare genetic variants on lipid response to a high-fat meal challenge and fenofibrate (FFB) therapy in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) cohort using an exome-wide sequencing-based association study. Our results showed that the rare coding variants in ITGA7, SIPA1L2, and CEP72 are significantly associated with fasting LDL cholesterol response to FFB (P = 1.24E-07), triglyceride postprandial area under the increase (AUI) (P = 2.31E-06), and triglyceride postprandial AUI response to FFB (P = 1.88E-06), respectively. We sought to replicate the association for SIPA1L2 in the Heredity and Phenotype Intervention (HAPI) Heart Study, which included a high-fat meal challenge but not FFB treatment. The associated rare variants in GOLDN were not observed in the HAPI Heart study, and thus the gene-based result was not replicated. For functional validation, we found that gene transcript level of SIPA1L2 is associated with triglyceride postprandial AUI (P < 0.05) in GOLDN. Our study suggests unique genetic mechanisms contributing to the lipid response to the high-fat meal challenge and FFB therapy.

scholarly journals Genomics of Postprandial Lipidomics in the Genetics of Lipid-Lowering Drugs and Diet Network Study

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4000
Author(s):  
Marguerite R. Irvin ◽  
May E. Montasser ◽  
Tobias Kind ◽  
Sili Fan ◽  
Dinesh K. Barupal ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Fatty Acid ◽  
Fatty Acid Desaturase ◽  
Lipid Lowering ◽  
Chromosome 11 ◽  
High Fat ◽  
Lipid Lowering Drugs ◽  
Lipid Species ◽  
Lipid Response ◽  
Fat Meal

Postprandial lipemia (PPL) is an important risk factor for cardiovascular disease. Inter-individual variation in the dietary response to a meal is known to be influenced by genetic factors, yet genes that dictate variation in postprandial lipids are not completely characterized. Genetic studies of the plasma lipidome can help to better understand postprandial metabolism by isolating lipid molecular species which are more closely related to the genome. We measured the plasma lipidome at fasting and 6 h after a standardized high-fat meal in 668 participants from the Genetics of Lipid-Lowering Drugs and Diet Network study (GOLDN) using ultra-performance liquid chromatography coupled to (quadrupole) time-of-flight mass spectrometry. A total of 413 unique lipids were identified. Heritable and responsive lipid species were examined for association with single-nucleotide polymorphisms (SNPs) genotyped on the Affymetrix 6.0 array. The most statistically significant SNP findings were replicated in the Amish Heredity and Phenotype Intervention (HAPI) Heart Study. We further followed up findings from GOLDN with a regional analysis of cytosine-phosphate-guanine (CpGs) sites measured on the Illumina HumanMethylation450 array. A total of 132 lipids were both responsive to the meal challenge and heritable in the GOLDN study. After correction for multiple testing of 132 lipids (α = 5 × 10−8/132 = 4 × 10−10), no SNP was statistically significantly associated with any lipid response. Four SNPs in the region of a known lipid locus (fatty acid desaturase 1 and 2/FADS1 and FADS2) on chromosome 11 had p < 8.0 × 10−7 for arachidonic acid FA(20:4). Those SNPs replicated in HAPI Heart with p < 3.3 × 10−3. CpGs around the FADS1/2 region were associated with arachidonic acid and the relationship of one SNP was partially mediated by a CpG (p = 0.005). Both SNPs and CpGs from the fatty acid desaturase region on chromosome 11 contribute jointly and independently to the diet response to a high-fat meal.

Effects of a High-Carb vs. High-Fat Meal on Glycemia, Insulin, Interleukin-6, TNF-Alpha, and Apo-B

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 265-LB ◽  
Author(s):  
HELMUT O. STEINBERG ◽  
FRANKIE B. STENTZ ◽  
NANDITA K. SHANKAR
Keyword(s):  
Interleukin 6 ◽  
Tnf Alpha ◽  
High Fat ◽  
Apo B ◽  
Fat Meal

162-LB: Impact of High-Fat Meal on Circulating microRNA in Youth with T1DM

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 162-LB
Author(s):  
JEANIE B. TRYGGESTAD ◽  
APRIL M. TEAGUE ◽  
KEVIN R. SHORT
Keyword(s):  
Circulating Microrna ◽  
High Fat ◽  
Fat Meal

scholarly journals Central and peripheral arterial stiffness responses to uninterrupted prolonged sitting combined with a high-fat meal: a randomized controlled crossover trial

2021 ◽  
Author(s):  
Simon Fryer ◽  
Keeron Stone ◽  
Craig Paterson ◽  
Meghan Brown ◽  
James Faulkner ◽  
...  
Keyword(s):  
Arterial Stiffness ◽  
Cardiovascular Health ◽  
Pulse Wave ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
High Fat ◽  
Low Fat ◽  
Peripheral Arterial ◽  
Fat Meal ◽  
Over Time

AbstractIndependently, prolonged uninterrupted sitting and the consumption of a meal high in saturated fats acutely disrupt normal cardiovascular function. Currently, the acute effects of these behaviors performed in combination on arterial stiffness, a marker of cardiovascular health, are unknown. This study sought to determine the effect of consuming a high-fat meal (Δ = 51 g fat) in conjunction with prolonged uninterrupted sitting (180 min) on measures of central and peripheral arterial stiffness. Using a randomized crossover design, 13 young healthy males consumed a high-fat (61 g) or low-fat (10 g) meal before 180 min of uninterrupted sitting. Carotid-femoral (cf) and femoral-ankle (fa) pulse wave velocity (PWV), aortic-femoral stiffness gradient (af-SG), superficial femoral PWV beta (β), and oscillometric pulse wave analysis outcomes were assessed pre and post sitting. cfPWV increased significantly more following the high-fat (mean difference [MD] = 0.59 m·s−1) meal than following the low-fat (MD = 0.2 m·s−1) meal, with no change in faPWV in either condition. The af-SG significantly decreased (worsened) (ηp2 = 0.569) over time in the high- and low-fat conditions (ratio = 0.1 and 0.1, respectively). Superficial femoral PWVβ significantly increased over time in the high- and low-fat conditions (ηp2 = 0.321; 0.8 and 0.4 m·s−1, respectively). Triglycerides increased over time in the high-fat trial only (ηp2 = 0.761). There were no significant changes in blood pressure. Consuming a high-fat meal prior to 180 min of uninterrupted sitting augments markers of cardiovascular disease risk more than consuming a low-fat meal prior to sitting.

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