Open Access Research

Differential effects of dietary protein sources on postprandial low-grade inflammation after a single high fat meal in obese non-diabetic subjects

Jens Holmer-Jensen1*, Toni Karhu2, Lene S Mortensen1, Steen B Pedersen1, Karl-Heinz Herzig2 and Kjeld Hermansen1

Author Affiliations

1 Department of Endocrinology and Metabolism MEA, Aarhus University Hospital, Aarhus, Denmark

2 Institute of Biomedicine and Biocenter of Oulu Faculty of Medicine, Finland

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Nutrition Journal 2011, 10:115  doi:10.1186/1475-2891-10-115

Published: 19 October 2011

Abstract

Background

Obesity is a state of chronic low-grade inflammation. Chronic low-grade inflammation is associated with the pathophysiology of both type-2 diabetes and atherosclerosis. Prevention or reduction of chronic low-grade inflammation may be advantageous in relation to obesity related co-morbidity. In this study we investigated the acute effect of dietary protein sources on postprandial low-grade inflammatory markers after a high-fat meal in obese non-diabetic subjects.

Methods

We conducted a randomized, acute clinical intervention study in a crossover design. We supplemented a fat rich mixed meal with one of four dietary proteins - cod protein, whey isolate, gluten or casein. 11 obese non-diabetic subjects (age: 40-68, BMI: 30.3-42.0 kg/m2) participated and blood samples were drawn in the 4 h postprandial period. Adiponectin was estimated by ELISA methods and cytokines were analyzed by multiplex assay.

Results

MCP-1 and CCL5/RANTES displayed significant postprandial dynamics. CCL5/RANTES initially increased after all meals, but overall CCL5/RANTES incremental area under the curve (iAUC) was significantly lower after the whey meal compared with the cod and casein meals (P = 0.0053). MCP-1 was initially suppressed after all protein meals. However, the iAUC was significantly higher after whey meal compared to the cod and gluten meals (P = 0.04).

Conclusion

We have demonstrated acute differential effects on postprandial low grade inflammation of four dietary proteins in obese non-diabetic subjects. CCL5/RANTES initially increased after all meals but the smallest overall postprandial increase was observed after the whey meal. MCP-1 was initially suppressed after all 4 protein meals and the whey meal caused the smallest overall postprandial suppression.

Trial Registration

ClinicalTrials.gov ID: NCT00863564

Keywords:
obesity; metabolic syndrome; dietary protein; nutrition; inflammation; cytokines; postprandial period