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

Kim-Tiu Teng,Lin Faun Chang,Kalanithi Nesaretnam,Chee-Yan Chang

doi:10.1186/1475-2891-13-12

Kim-Tiu Teng, Lin Faun Chang + Show 2 more

Open Access

https://doi.org/10.1186/1475-2891-13-12

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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.

Highlights

Obesity is a global epidemic in both developed and developing countries
The disrupted Toll-like receptors (TLR)-4 signalling pathways lead to the inhibition of Nuclear factor-kappa B (NF-κB) resulting in the downregulation of inflammatory responses [53,54]. These findings indicate that the intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) reduces the secretion of pro-inflammatory cytokines, and it may be possible that these n-3 polyunsaturated fatty acids (PUFA) play a role in preventing macrophage infiltration into adipose tissue [50]
HFM, high fat meal; LFM, low fat meal; Saturated fatty acids (SFA), saturated fats; Monounsaturated fats (MUFA), monounsaturated fats; PUFA, polyunsaturated fats; % en, percentage energy; IL, interleukin; High-sensitivity C-reactive protein (hsCRP), high-sensitivity C-reactive protein; tumor necrosis factor-α (TNF-α), tumor necrosis factor- alpha; sICAM-1, soluble intracellular adhesion molecule-1; sVCAM-1, soluble vascular adhesion molecule-1; HMW, high molecular weight; AUC, area under the curve; ROS, reactive oxygen species; NF-κB, nuclear factor kappa-β; ↓, reduced postprandial concentrations; ↑, increased postprandial concentrations; =, no postprandial/after meal effect; ↑↑, higher postprandial increment compared to other meals; NS, no significant difference between meals

Summary

Introduction

Obesity is a global epidemic in both developed and developing countries. In the United States alone, it is estimated that approximately 69% of adults are overweight (BMI ≥25 kg/m2) and 36% are obese (BMI ≥30 kg/m2) [1]. The disrupted TLR-4 signalling pathways lead to the inhibition of NF-κB resulting in the downregulation of inflammatory responses [53,54] These findings indicate that the intake of EPA and DHA reduces the secretion of pro-inflammatory cytokines, and it may be possible that these n-3 PUFA play a role in preventing macrophage infiltration into adipose tissue [50]. Type of dietary fats on postprandial inflammatory response Masson and Mensink [67] reported that in 13 overweight men, plasma IL-6, TNF-α and soluble vascular adhesion molecule-1 (sVCAM-1) concentrations decreased after n-6 PUFA meal, while the markers were increased after SFA meal (Table 2).

Design Dietary intervention

Strengths and limitations

Findings

Conclusion