British Journal of Nutrition

Full Papers

Dietary factors and low-grade inflammation in relation to overweight and obesity

Philip C. Caldera1, Namanjeet Ahluwaliaa2, Fred Brounsa3a21, Timo Buetlera4a22, Karine Clementa5, Karen Cunninghama6, Katherine Espositoa7, Lena S. Jönssona8, Hubert Kolba9, Mirian Lansinka10, Ascension Marcosa11, Andrew Margiorisa12, Nathan Matusheskia13, Herve Nordmanna14, John O'Briena4, Giuseppe Pugliesea15, Salwa Rizkallaa5, Casper Schalkwijka16, Jaakko Tuomilehtoa17, Julia Wärnberga11a18, Bernhard Watzla19 and Brigitte M. Winklhofer-Rooba20

a1 School of Medicine, University of Southampton, Southampton SO16 6YD, UK

a2 INSERM U557, University of Paris, 93017 Bobigny Cedex, France

a3 Cargill R&D Centre Europe, 1800 Vilvoorde, Belgium

a4 Nestlé Research Centre, Vers-chez-les-Blanc, 1000 Lausanne, Switzerland

a5 Department of Nutrition, INSERM U872, Research Center on Human Nutrition, Pitie Salpetriere Hospital, 75013 Paris, France

a6 Coca-Cola Europe, Hammersmith, London W6 9HQ, UK

a7 Division of Metabolic Diseases, University of Naples, 80138 Naples, Italy

a8 ILSI Europe a.i.s.b.l., Avenue E. Mounier 83, Box 6, 1200 Brussels, Belgium

a9 Research Group Immunobiology, Medical Faculty, University of Dusseldorf, 40225 Dusseldorf, Germany

a10 Danone Research, Centre for Specialised Nutrition, 6700, CA, Wageningen, The Netherlands

a11 Department of Metabolism and Nutrition, CSIC, Spanish National Research Council, 28040 Madrid, Spain

a12 School of Medicine, University of Crete, 71409 Heraklion, Greece

a13 Nutrition Research, Kraft Foods, Inc., Glenview IL 60025, USA

a14 Ajinomoto Europe, 75817 Paris, France

a15 Department of Clinical and Molecular Medicine, “La Sapienza” University of Rome, 00161 Rome, Italy

a16 Internal Medicine, University of Maastricht, 6202 AZ Maastricht, The Netherlands

a17 University of Helsinki, 00014 Helsinki, Finland

a18 Department of Preventive Medicine and Public Health, University of Navarra, 31080- Pamplona, Spain

a19 Max-Rubner Institut, Federal Research Centre for Nutrition and Food, 76131 Karlsruhe, Germany

a20 Institute of Molecular Biosciences, Human Nutrition and Metabolism Research and Training Center, Karl-Franzens University of Graz, 8010 Graz, Austria

a21 Department of Nutrition, Maastricht University Medical Centre, 6200 MD Maastricht, The Netherlands

a22 XeRR, Institute of Pharmacology and Toxicology, University of Zürich, 8057 Zürich, Switzerland

Abstract

Low-grade inflammation is a characteristic of the obese state, and adipose tissue releases many inflammatory mediators. The source of these mediators within adipose tissue is not clear, but infiltrating macrophages seem to be especially important, although adipocytes themselves play a role. Obese people have higher circulating concentrations of many inflammatory markers than lean people do, and these are believed to play a role in causing insulin resistance and other metabolic disturbances. Blood concentrations of inflammatory markers are lowered following weight loss. In the hours following the consumption of a meal, there is an elevation in the concentrations of inflammatory mediators in the bloodstream, which is exaggerated in obese subjects and in type 2 diabetics. Both high-glucose and high-fat meals may induce postprandial inflammation, and this is exaggerated by a high meal content of advanced glycation end products (AGE) and partly ablated by inclusion of certain antioxidants or antioxidant-containing foods within the meal. Healthy eating patterns are associated with lower circulating concentrations of inflammatory markers. Among the components of a healthy diet, whole grains, vegetables and fruits, and fish are all associated with lower inflammation. AGE are associated with enhanced oxidative stress and inflammation. SFA and trans-MUFA are pro-inflammatory, while PUFA, especially long-chain n-3 PUFA, are anti-inflammatory. Hyperglycaemia induces both postprandial and chronic low-grade inflammation. Vitamin C, vitamin E and carotenoids decrease the circulating concentrations of inflammatory markers. Potential mechanisms are described and research gaps, which limit our understanding of the interaction between diet and postprandial and chronic low-grade inflammation, are identified.

(Received January 20 2011)

(Revised August 08 2011)

(Accepted September 07 2011)

Correspondence:

c1 Correspondence: ILSI Europe a.i.s.b.l., Avenue E. Mounier 83, Box 6 – 1200 Brussels, Belgium, fax +32 2 762 00 44, email publications@ilsieurope.be

Footnotes

Abbreviations: AGE, advanced glycation end products; AGE-R, advanced glycation end product receptor; AHEI, alternate healthy eating index; ALE, advanced lipoxidation end products; CCL, chemokine (C–C motif) ligand; CCR, CC chemokine receptor; CFU, colony forming units; CLA, conjugated linoleic acids; CRP, C-reactive protein; DQI, Diet Quality Index; DQI-R, revised Diet Quality Index; GI, glycaemic index; GL, glycaemic load; HEI, healthy eating index; IFN, interferon; IL-1ra, IL-1 receptor antagonist; IRS, insulin receptor substrate; LPS, lipopolysaccharide; MAPK, mitogen-activated protein kinase; MCP, monocyte chemoattractant protein; MIF, macrophage migration inhibitory factor; MIP, macrophage inflammatory protein; MRP, Maillard reaction products; NHANES, National Health and Nutrition Examination Survey; PAI-1, plasminogen activator inhibitor 1; Q, quintile; RAGE, receptor for advanced glycation end products; RANTES, regulated on activation, normal T expressed and secreted; ROS, reactive oxygen species; SAA, serum amyloid A; sE-selectin, soluble E-selectin; sICAM-1, soluble intercellular adhesion molecule-1; sP-selectin, soluble P-selectin; STAMP, six-transmembrane protein of prostate; sTNFR, soluble receptors of TNF; sVCAM-1, soluble vascular cell adhesion molecule-1; TGF, transforming growth factor; TLR, Toll-like receptors

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