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The incidence of obesity and associated disorders has dramatically increased worldwide. Obese individuals exhibit an increased risk of developing diseases such as atherosclerosis, diabetes, non-alcoholic fatty liver disease and cancer. Breast, prostate or colorectal cancer (CRC) are leading cancers in the Western world. Epidemiological studies indicate that obesity represents a significant risk factor for the development of these cancers, although the exact mechanisms have not yet been identified. Research in the past years has characterised important pathways that link metabolism with the immune system and vice versa.1 Although, currently, there is still limited evidence, inflammatory/immune mediators released by many cell types including adipocytes could be attractive candidates for linking obesity with cancer. Two reports in this issue of Gut (see pages 1583 and 1637) provide further evidence that molecules regulating metabolic/inflammatory pathways might be involved in gastrointestinal carcinogenesis.2 3
Adipocytokines: key immune mediators derived mainly from adipocytes
Obesity is associated with a chronic inflammatory state characterised by abnormal cytokine and acute-phase protein production, and increased activity of inflammatory signalling pathways. Many of the interactions between metabolic and immune pathways are mediated by a complex network of soluble mediators derived from immune cells and adipocytes, ie, adipocytokines. Adiponectin and leptin are the most abundant adipocytokines produced by adipocytes.
Adiponectin is a pleiotropic molecule with immunomodulatory, anti-inflammatory, …
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