Both diabetes and cancer are amongst the most serious medical conditions in the United States, requiring billions of dollars of treatment each and every year. Though doctors are no stranger to these diseases, the relationship between the two is not completely understood. A 2019 study has shed some much-needed light on this important topic.
Under the Microscope
This report was presented at the 2019 national meeting of the American Chemical Society (ACS). For this project, the study authors examined the DNA in both laboratory-grown tissue samples and in rodent models. Specifically, the team paid close attention to parts of their DNA structures known as adducts, or DNA bases that had been chemically modified. The study authors wanted to determine if these structures had sustained damage due to diabetes.
The team noticed that their diabetic tissue samples had a high frequency of a certain type of DNA adduct, known as N2-(1-carboxyethyl)-2′-deoxyguanosine, or CEdG for short. This same pattern was likewise observed amongst the study’s rodent subjects. In other words, diabetes caused both the lab-grown tissue samples and mice to suffer significant DNA damage. In theory, such damage could cause instability within a human being’s DNA, leading to the development of cancerous cells.
The Power of Protein
The study authors attributed this development to the behavior of two proteins, called HIF1a and mTORC1. Both proteins became noticeably less active thanks to the onset of diabetes. HIF1a in particular is an important protein, as it stimulates genes involved with the body’s self-repair capabilities.
Given the study’s findings, the authors contend that drugs used to boost the activity of HIF1a or mTORC1 proteins might have a positive impact on diabetic animal models. If they are indeed correct, this would mean that such testing subjects would face a reduced risk of cancer. The authors further stated that should they achieve this goal with animal subjects, testing involving human participants would follow.
