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Medicine
Friday, July 20, 2018
/ natchas, stockadobecom
Sydney and Boston – Diabetics have a slightly increased risk of cancer, according to the recent meta-badysis of Diabetologia ( 2018, doi: 10.1007 / s00125-018-4664-5) is slightly more pronounced for women than for men. Experiments published in Nature (2018, doi: 10.1038 / s41586-018-0350-5) provide a possible explanation.
Various epidemiological studies have come to the conclusion in recent years that diabetics more often than others develop cancerous tumors in the stomach, lungs, kidneys, esophagus, intestines, pancreas, bladder and thyroid gland. The data presented by Toshiaki Ohkuma and the employees of the George Institute for Global Health in Sydney confirm this. Their meta-badysis of 121 cohort studies with more than 19 million participants shows for the first time that the risk is slightly higher for women than for men.
Women with diabetes are 27% more likely to develop cancer in their lifetime than women without diabetes (adjusted relative risk of 1.27, 95% confidence interval from 1.21 to 1.32). For men with diabetes, it increased only 19% (RR 1.19, 1.13-1.25). The gender difference of 6% was also significant (relative risk rate 1.06, 1.03-1.09).
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Specifically, women with diabetes were 11% more likely to develop kidney cancer, up to 13% more common in oral cancer, 14% more likely to have gastric cancer and 15% more likely to have leukemia than men with diabetes. The only exception was liver cancer, which was 12% less common among women with diabetes than men with diabetes.
One can only question gender-related causes. However, previous studies have shown that blood glucose in women with diabetes is often worse than in men with diabetes, which is due to less adherence to the drug. The longer life expectancy of women and therefore the longer duration of hyperglycemia could play a role.
Why diabetics more often develop cancer is not exactly known. Most experts suspect that hyperglycemia is central. One hypothesis is that glucose affects the methylation of DNA, which can affect the activity of a variety of genes.
A team led by Yujiang Shi of Harvard Medical School, Boston, studied this for blood cells. Culture of cells in medium with increased glucose concentration reduced the proportion of 5-hydroxymethylcytosine (5hmC), the methylated version of the nucleoside cytosine on DNA. Researchers attribute this to reduced activity of the TET2 enzyme, which is also clbadified as a tumor suppressor because it can prevent the development of cancer cells.
Interestingly, the activity of TET2 is regulated by the enzyme AMPK (AMP-activated protein kinase). It is now known that antidiabetic metformin achieves its hypoglycemic effect by activating AMPK. Epidemiological studies suggest that metformin may reduce the risk of cancer.
Shi therefore studied the effects of TET2 and metformin on mice. In animals, diabetes was first caused by the injection of streptozotocin. Later, the animals were injected with human melanoma cells. Tumor growth could be reduced by activating TET2, but also by treatment with metformin.
The results of the study provide not only a biologically plausible explanation for the increased risk of cancer in diabetics, but they also confirm that metformin is one of the most used. has an anti-cancer effect. The extent to which this protective effect is pronounced in the treatment of diabetics should ideally be studied in clinical trials. Epidemiological studies can only provide initial clues here.
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