title: Dietary factors and low-grade inflammation in relation to overweight and obesity.
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.
authors: School of Medicine, University of Southampton, Southampton, UK.
authors: Philip C
authors: PC
authors: Calder
authors: Namanjeet
authors: N
authors: Ahluwalia
authors: Fred
authors: F
authors: Brouns
authors: Timo
authors: T
authors: Buetler
authors: Karine
authors: K
authors: Clement
authors: Karen
authors: K
authors: Cunningham
authors: Katherine
authors: K
authors: Esposito
authors: Lena S
authors: LS
authors: Jönsson
authors: Hubert
authors: H
authors: Kolb
authors: Mirian
authors: M
authors: Lansink
authors: Ascension
authors: A
authors: Marcos
authors: Andrew
authors: A
authors: Margioris
authors: Nathan
authors: N
authors: Matusheski
authors: Herve
authors: H
authors: Nordmann
authors: John
authors: J
authors: O'Brien
authors: Giuseppe
authors: G
authors: Pugliese
authors: Salwa
authors: S
authors: Rizkalla
authors: Casper
authors: C
authors: Schalkwijk
authors: Jaakko
authors: J
authors: Tuomilehto
authors: Julia
authors: J
authors: Wärnberg
authors: Bernhard
authors: B
authors: Watzl
authors: Brigitte M
authors: BM
authors: Winklhofer-Roob
mesh_terms: D000375:Aging; D000818:Animals; D004032:Diet / Q000009:adverse effects; D005511:Food Handling; D017127:Glycation End Products, Advanced / Q000009:adverse effects / Q000097:blood / Q000378:metabolism; D006801:Humans; D007333:Insulin Resistance; D015227:Lipid Peroxidation; D009043:Motor Activity; D009765:Obesity / Q000097:blood / Q000209:etiology* / Q000276:immunology* / Q000378:metabolism; D050177:Overweight / Q000097:blood / Q000209:etiology* / Q000276:immunology* / Q000378:metabolism; D010545:Peroxides / Q000009:adverse effects
chemical_list: D017127:Glycation End Products, Advanced; D010545:Peroxides