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Original Research

Modulatory Role of Omentin-1 in Inflammation: Cytokines and Dietary Intake

, MSPH, , PhD, , PhD & , MD, PhD
Pages 670-678 | Received 13 Jul 2015, Accepted 23 Nov 2015, Published online: 22 Jun 2016
 

Abstract

Purpose: Obesity is known as a chronic inflammatory state whereby anti-inflammatory adipokines, such as omentin-1 levels, are decreased. The present study aims to determine omentin-1 levels in relation to dietary intake, inflammation, and immune response in healthy obese individuals.

Method: A total of 170 obese participants (body mass index [BMI] ≥ 30) were recruited in this cross-sectional study. Body composition was evaluated by a body composition analyzer, and inflammatory markers (high-sensitivity C-reactive protein [hs-CRP], interleukin (IL)-4, IL-6, IL-1β, IL-17, IL-10, IL-13, and tumor necrosis factor-alpha [TNF-α]) were measured by enzyme-linked immunosorbent assay (ELISA) kits.

Results: We observed associations between higher serum levels of omentin-1 and lower levels of fasting insulin, glucose, total cholesterol, IL-6, and TNF-α concentrations; higher levels of IL-13, IL-4, and IL-1β were associated with higher serum levels of omentin-1 (all p < 0.05). Omentin-1 levels were not associated with IL-10, hs-CRP, and IL-17 concentrations. We also observed associations between higher intake of saturated fatty acid (SFA) and omentin-1 levels, even after adjustment for total energy intake (p = 0.04). Women with low intake of SFA had higher levels of omentin-1 (p = 0.03); a similar relation was not observed in men.

Conclusion: Omentin-1 has an anti-inflammatory role in obesity and exerts its effects probably by inducing an increase in Th-2 cytokines comprising IL-13 and IL-4. Omentin-1 is not related to IL-17, a regulatory T cell cytokine, which modulates T helper balance. Levels of inflammatory cytokines are decreased in higher concentrations of omentin-1, except IL-1β. Lower intake of SFA may modify omentin-1 levels in women. Our study demonstrated the probable protective role of omentin-1 in obesity-related inflammation and insulin resistance.

ACKNOWLEDGMENTS

The authors thank Dr. Hassan S. Dashti for his input. We are grateful to all of the participants for their contribution to this research. This study was approved by a local Ethics Committee of Tehran University of Medical Sciences. All participants signed a written informed consent that was approved by this committee prior to enrollment in the study.

Funding

This study was supported by grants from the Tehran University of Medical Sciences (TUMS) Tehran, Iran (Grant ID: 94-01-161-28473).

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