Chronic Kidney disease may be explained by epigenetic changes.

is defined by the changes to gene expression caused through outside influences such as the environment or food ingested, and not directly through changes in the DNA sequence. A new study published in the Biology journal found that a pattern of chemical modification on DNA methylation affects gene expression in cells from patients with chronic disease versus healthy controls. Approximately 10 % of people or more than 20 million, aged 20 years or older in the have chronic disease, according to the Centers for Disease Control (CDC).

Chronic disease is considered to be a serious disease and is defined as a condition in which the kidneys are damaged and cannot adequately filter blood. The end result of the chronic condition is that it causes waste to build up, which leads to other problems, including , , and bone disease.

cells have been associated with having a past metabolic effect, i.e. they remember the conditions that a specific disease such as diabetes imposes on them. “This is called the metabolic memory effect,” says Susztak, a lead study author. “ cells remember the past bad metabolic environment.”

“Most of the research on so far has been on promoter regions on cancer cells,” says Susztak. “The difference we found in dysregulation between the two cell populations may indicate that dysregulation in cancer is different from dysregulation in chronic disease. Five years ago there was no epigenetic information outside of cancer,” says Susztak.

The study results and the influence of epigentics on a chronic disease raises the possibility of identifying new and treatment methods associated with the condition.

Source

Yi-An Ko, Davoud Mohtat, Masako Suzuki, Ae Park, Maria Izquierdo, Sang Han, Hyun Kang, Han Si, Thomas Hostetter, James M Pullman, Melissa Fazzari, Amit Verma, Deyou Zheng, John M Greally, Katalin Susztak. Cytosine methylation changes in enhancer regions of core pro-fibrotic characterize fibrosis development. Biology, 2013; 14 (10): R108 DOI: 10.1186/gb-2013-14-10-r108

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