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Leptin A Potential Link To Colon Cancer

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Tests on three human colon cancer cell lines showed that the fat-hormone 'leptin' may enhance the growth of colonic cancers. This finding could show why obese people are at increased risk of colon cancer. It could also point to new modes of treating this type of cancer, finds research from the University of California, San Diego School of Medicine, published today in BJS.

Leptin is a hormone that is released from fat cells (adipocytes) the more fat you have, the more leptin will be in your blood stream. This hormone plays an important role in regulating bodyweight and energy expenditure.People who are obese have a two to three fold increased risk of developing colon cancer compared to similar normal-weight individuals. Research has also revealed that some colon cancer cells carry receptors for leptin.The question is whether there is any evidence that these receptors could respond to increased levels of leptin that are caused by the obesity, and trigger the colon cancer cells to start dividing and growing. Now research shows that this may well be the case."These results may explain why obesity increases a person's risk of colonic cancer, and the fact that we have shown how leptin stimulates these cells means that drug companies may be in a better position to develop new treatments against the disease," says research co-author Dr Kim Barrett.By culturing cancer cells in a laboratory, they found that leptin could stimulate growth. In two out of three cell lines, leptin also prevented the sort of programmed cell death (apoptosis) that allows for the orderly death of normal cells, but when reduced, can contribute to cancer.The researchers then went on to reveal many of the signalling pathways that leptin affected in the cell. This showed that leptin does indeed interfere with many known intra-cellular systems that influence cancer cells.(Source: British Journal of Surgery (BJS) : University of California, San Diego : February 2007.)


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Posted On: 29 January, 2007
Modified On: 16 January, 2014

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