Modulation of obesity-induced inflammation by dietary fats: mechanisms and clinical evidence - PubMed (original) (raw)

Review

Modulation of obesity-induced inflammation by dietary fats: mechanisms and clinical evidence

Kim-Tiu Teng et al. Nutr J. 2014.

Abstract

Obesity plays a pivotal role in the development of low-grade inflammation. Dietary fatty acids are important modulators of inflammatory responses. Saturated fatty acids (SFA) and n-6 polyunsaturated fatty acids (PUFA) have been reported to exert pro-inflammatory effects. n-3 PUFA in particular, possess anti-inflammatory properties. Numerous clinical studies have been conducted over decades to investigate the impact of dietary fatty acids on inflammatory response in obese individuals, however the findings remained uncertain. High fat meals have been reported to increase pro-inflammatory responses, however there is limited evidence to support the role of individual dietary fatty acids in a postprandial state. Evidence in chronic studies is contradictory, the effects of individual dietary fatty acids deserves further attention. Weight loss rather than n-3 PUFA supplementation may play a more prominent role in alleviating low grade inflammation. In this context, the present review provides an update on the mechanistic insight and the influence of dietary fats on low grade inflammation, based on clinical evidence from acute and chronic clinical studies in obese and overweight individuals.

PubMed Disclaimer

Figures

Figure 1

Figure 1

TLR-4, toll-like-receptor 4; SFA, saturated fatty acids. SFA stimulate inflammation through TLR-4 dependent and independent pathways.

Figure 2

Figure 2

Dotted line, inhibit; solid line, activate. EPA, eicosapentaenoic acid; DHA, docosahexaenoic acid; GPR120, G protein-coupled receptor 120; JNK, JUN NH2-terminal kinase; TLR-4, toll-like-receptor 4; NF-κB, nuclear factor kappa-β; PPARγ, peroxisome proliferator-activated receptor γ; AA, arachidonic acid; PGE2, prostaglandins E2. Anti-inflammatory mechanisms of EPA and DHA. EPA and DHA inhibit NF-κB and JNK through binding with GPR120. Incorporation of these n-3 PUFA disrupts the translocation of TLR-4 into lipid raft, thus inactivates NF-κB pathway. Besides, EPA and DHA interfere with the TLR-4 signaling pathway via the downregulation of NADPH oxidase production, which results in the inhibition of NF-κB pathway. These fatty acids also activate PPARγ and, result in the upregulation of adiponectin and leptin secretion. In addition, the intake of EPA and DHA leads to antagonism of n-6 fatty acid arachidonic acid (AA).

Similar articles

Cited by

References

    1. Flegal KM, Carroll MD, Kit BK, Ogden CL. Prevalence of obesity and trends in the distribution of body mass index among US adults, 1999–2010. JAMA. 2012;307:491–497. - PubMed
    1. Olson NC, Callas PW, Hanley AJ, Festa A, Haffner SM, Wagenknecht LE, Tracy RP. Circulating levels of TNF-alpha are associated with impaired glucose tolerance, increased insulin resistance, and ethnicity: the insulin resistance atherosclerosis study. J Clin Endocrinol Metab. 2012;97:1032–1040. - PMC - PubMed
    1. Bose KS, Gupta SK, Vyas P. Adipocytokine levels in genetically high risk for type 2 diabetes in the Indian population: a cross-sectional study. Exp Diabetes Res. 2012;2012:386524. - PMC - PubMed
    1. Gelaye B, Revilla L, Lopez T, Suarez L, Sanchez SE, Hevner K, Fitzpatrick AL, Williams MA. Association between insulin resistance and c-reactive protein among Peruvian adults. Diabetol Metab Syndr. 2010;2:30. - PMC - PubMed
    1. Jellema A, Plat J, Mensink RP. Weight reduction, but not a moderate intake of fish oil, lowers concentrations of inflammatory markers and PAI-1 antigen in obese men during the fasting and postprandial state. Eur J Clin Invest. 2004;34:766–773. - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources