Obesity has emerged as a leading environmental risk factor for the development of CRC. However, the mechanisms underlying this relationship have not yet been fully explained. Recent literature has focused on 1) inflammatory processes, 2) adipokines, and 3) estrogen. Obesity-enhanced inflammation is largely orchestrated by increases in adipose tissue macrophages leading to the secretion of TNF-alpha, MCP-1, and IL-6, all of which are linked to CRC. Adiponectin is decreased with obesity and has been reported to be negatively associated with CRC, while leptin, which is increased, is positively associated with the disease. Estrogen has been shown to influence CRC, although its role remains controversial; some studies have implicated estrogen as being protective, while others have suggested it to be a risk factor. We highlight the most important recent advances that have been made on the aforementioned mechanisms that are thought to link obesity to CRC.
|Commitee:||Fan, Daping, Singh, Udai|
|School:||University of South Carolina|
|School Location:||United States -- South Carolina|
|Source:||MAI 51/06M(E), Masters Abstracts International|
|Subjects:||Microbiology, Medicine, Immunology|
|Keywords:||Adipokines, Colorectal cancer, Estrogen, Inflammation, Obesity|
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