» Articles » PMID: 22810465

Antioxidant and Inflammatory Response Following High-fat Meal Consumption in Overweight Subjects

Overview
Journal Eur J Nutr
Date 2012 Jul 20
PMID 22810465
Citations 23
Authors
Affiliations
Soon will be listed here.
Abstract

Purpose: Postprandial metabolic stress as a consequence of ingestion of high-energy meals is recognized as an important risk factor for cardiovascular disease. The objective of this study was to evaluate the inflammatory and antioxidant response of the body to the acute ingestion of a high-fat meal (HFM).

Methods: Fifteen healthy overweight subjects were recruited for the study. After HFM consumption, plasma glucose, insulin, uric acid (UA), triglycerides (TG), total cholesterol (TC), thiols (SH), inflammatory cytokines (IL-6 and TNF-α) and dietary antioxidants were measured at 0, 0, 5, 1, 2, 4, 6 and 8 h points from ingestion.

Results: The ingestion of HFM induced significant increases in both TG and TC, with peaks at 4 h (p < 0.001) and 8 h (p < 0.01), respectively. IL-6 and TNF-α significantly increased postprandially, reaching maximum concentrations 8 h after meal consumption (p < 0.001). Whereas plasma concentrations of vitamins and carotenoids were not changed by HFM, SH and UA increased, peaking 2-4 h postingestion (p < 0.001 and 0.01, respectively). Increments of SH and UA were positively correlated with AUC for TG (Pearson coefficient 0.888, p < 0.001 and 0.923, p < 0.001, respectively).

Conclusions: Present results indicate that as a consequence of an excess of dietary fat, the body responds through an inflammatory reaction, which is accompanied by an increment of endogenous antioxidant defenses, mediated by UA and SH, but not by vitamins C and E and carotenoids. Although further studies are needed, results of the current investigation represent novel findings on endogenous strategies of redox defense from fat overloads.

Citing Articles

Dietary habit and risk of rheumatoid arthritis: a mendelian randomization study identifying protective and risk factors.

Li J, Xie X, Chen X, Xie L, Luo M, Yin M Eur J Nutr. 2024; 64(1):3.

PMID: 39535565 DOI: 10.1007/s00394-024-03518-4.


Circadian Modulation of the Antioxidant Effect of Grape Consumption: A Randomized Controlled Trial.

Blanton C, Ghimire B, Khajeh Pour S, Aghazadeh-Habashi A Int J Environ Res Public Health. 2023; 20(15).

PMID: 37569042 PMC: 10419126. DOI: 10.3390/ijerph20156502.


Beef intake and risk of rheumatoid arthritis: Insights from a cross-sectional study and two-sample Mendelian randomization.

Chen W, Liu K, Huang L, Mao Y, Wen C, Ye D Front Nutr. 2022; 9:923472.

PMID: 36147307 PMC: 9486088. DOI: 10.3389/fnut.2022.923472.


Endothelial Progenitor Cell Levels and Extent of Post-prandial Lipemic Response.

Akcan B, Orem A, Altinkaynak Y, Kural B, Orem C, Sonmez M Front Nutr. 2022; 9:822131.

PMID: 35237643 PMC: 8885282. DOI: 10.3389/fnut.2022.822131.


Goals in Nutrition Science 2020-2025.

Bassaganya-Riera J, Berry E, Blaak E, Burlingame B, le Coutre J, van Eden W Front Nutr. 2021; 7:606378.

PMID: 33665201 PMC: 7923694. DOI: 10.3389/fnut.2020.606378.


References
1.
Schafer F, Buettner G . Redox environment of the cell as viewed through the redox state of the glutathione disulfide/glutathione couple. Free Radic Biol Med. 2001; 30(11):1191-212. DOI: 10.1016/s0891-5849(01)00480-4. View

2.
Eberly L, Stamler J, Neaton J . Relation of triglyceride levels, fasting and nonfasting, to fatal and nonfatal coronary heart disease. Arch Intern Med. 2003; 163(9):1077-83. DOI: 10.1001/archinte.163.9.1077. View

3.
Ames B, Cathcart R, Schwiers E, Hochstein P . Uric acid provides an antioxidant defense in humans against oxidant- and radical-caused aging and cancer: a hypothesis. Proc Natl Acad Sci U S A. 1981; 78(11):6858-62. PMC: 349151. DOI: 10.1073/pnas.78.11.6858. View

4.
Feig D, Kang D, Nakagawa T, Mazzali M, Johnson R . Uric acid and hypertension. Curr Hypertens Rep. 2006; 8(2):111-5. DOI: 10.1007/s11906-006-0005-z. View

5.
Jones D, Mody Jr V, Carlson J, Lynn M, Sternberg Jr P . Redox analysis of human plasma allows separation of pro-oxidant events of aging from decline in antioxidant defenses. Free Radic Biol Med. 2002; 33(9):1290-300. DOI: 10.1016/s0891-5849(02)01040-7. View