The true cost of in-patient obesity: impact of obesity on inflammatory stress and morbidity.
The objective of the present review is to provide an overview of the metabolic effects of pro-inflammatory cytokine production during infection and injury; to highlight the disadvantages of pro-inflammatory cytokine production and inflammatory stress on morbidity and mortality of patients; to identify the influence of genetics and adiposity on inflammatory stress in patients and to indicate how nutrients may modulate the inflammatory response in patients. Recent research has shown clearly that adipose tissue actively secretes a wide range of pro- and anti-inflammatory cytokines. Paradoxically, although inflammation is an essential part of the response of the body to infection, surgery and trauma, it can adversely affect patient outcome. The metabolic effects of inflammation are mediated by pro-inflammatory cytokines. Metabolic effects include insulin insensitivity, hyperlipidaemia, muscle protein loss and oxidant stress. These effects, as well as being present during infective disease, are also present in diseases with a covert inflammatory basis. These latter diseases include obesity and type 2 diabetes mellitus. Inflammatory stress also increases during aging. The level of cytokine production, within individuals, is influenced by single nucleotide polymorphisms (SNP) in cytokine genes. The combination of SNP controls the relative level of inflammatory stress in both overt and covert inflammatory diseases. The impact of cytokine genotype on the intensity of inflammatory stress derived from an obese state is unknown. While studies remain to be done in the latter context, evidence shows that these genomic characteristics influence morbidity and mortality in infectious disease and diseases with an underlying inflammatory basis and thereby influence the cost of in-patient obesity. Antioxidants and n-3 PUFA alter the intensity of the inflammatory process. Recent studies show that genotypic factors influence the effectiveness of immunonutrients. A better understanding of this aspect of nutrient-gene interactions and of the genomic factors that influence the intensity of inflammation during disease will help in the more effective targeting of nutritional therapy.
Grimble
Robert F
RF
Institute of Human Nutrition, DOHaD Division, School of Medicine, University of Southampton, Mailpoint 887, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK. rfg1@soton.ac.uk
D000273:Adipose Tissue / Q000378:metabolism*; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007239:Infections / Q000276:immunology; D007249:Inflammation / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism; D008659:Metabolic Diseases / Q000209:etiology / Q000235:genetics / Q000378:metabolism; D018977:Micronutrients / Q000627:therapeutic use*; D054647:Nutrigenomics; D009765:Obesity / Q000150:complications* / Q000276:immunology; D020641:Polymorphism, Single Nucleotide; D014947:Wounds and Injuries / Q000276:immunology
D016207:Cytokines; D018977:Micronutrients