- Diabetes mellitus is a clinical syndrome characterized by high glucose in your blood
- High glucose levels damages DNA bases and suppress their repair
- Instability of genome leads to cancer
Introduction – Diabetes mellitus is a clinical syndrome which is characterized by hyperglicemia due to absolute or relative deficiency of insulin[1]. Insulin is a hormone produced by pancreas, its chemical messenger like function allows cells to absorb glucose from the blood, furthermore insulin regulates metabolism of carbohydrates, protein and fat[1][2]. Type 1 diabetes occurs due to destruction of insulin-secreting B cells in the pancreatic islets caused by T cell mediated autoimmune mechanisms which leads to profound insulin deficiency[1]. Type 2 diabetes is known as a more complex condition than type 1 because in addition to impaired pancreatic B-cell function, resistance of insulin in liver and muscle appears too[2].The resistance is caused due to release of large quantities of free fatty acids from metabolically active adipose tissue which compete with glucose as a fuel supply for oxidation in muscles.[1]. In addition to this, adipose-derived hormones such as leptin, adiponectin and resistin act on specific receptors in muscles and liver, affecting gluconeogenesis and hepatic lipid metabolism[1]. This body cell resistance of insulin results in increased insulin production from beta cells of pancreas leading to hyperinsulinemia[1].
Statistics – Since Diabetes as a chronic metabolic disease leads to serious damage to the organs such as heart, eyes, kidneys, vessels as well as nerves, it seems to be a growing challenge in the world. [4]. According to statistics, the most common type of diabetes is type 2 diabetes[4]. According to WHO, 422 million people around the world have diabetes nowadays. [6] It is estimated that by 2045, number of people with living with diabetes will rise 629 million [5]. Data are very concerning about cancer too; cancer as the second leading cause of death in the world is estimated to cause more than 9.6 million death in 2019[7].
Impact of high glucose on cancer development – One of the greatest challenge in the science was solving the mystery that confirms that people with diabetes have an increased risk of developing some forms of cancer such as: breast, ovarian, kidney cancer etc [8]. The latest study of American Chemical Society confirms the mechanism that solves the mystery of how diabetes can increase cancer risk [8]. Data found that high blood glucose is a damaging factor for DNA bases, since it causes chemical changes to them forming DNA adducts named N2(1-carboxyethyl)-2-deoxygasine (CEdG)[8]. People with diabetes had significantly higher levels of CedG than people without diabetes [8]. In addition to this, in people with diabetes, there were found two proteins known as transcriptor factor HIF1-alfa which activates several genes involved in the repair process as well as Mechanistic target of rapamycin complex 1 (mTORC1) protein which activates HIF1-alfa [8]. Both of them show less activity in people with diabetes, which allows adducts such as CEdG to not be fixed properly by the cells[8]. The future is bright since many tests are getting done in mixing drugs that stabilize HIF1 or enhance mTORC1 with antidiabetic drugs[8].
This exciting study leads to better solution in the future for people with diabetes to reduce their cancer risk!
COPYRIGHT: This article is the property of We Speak Science, a non-profit institution co-founded by Dr. Detina Zalli and Dr. Argita Zalli. The article is written by Rexhep Sahatçiu, University of Prishtina, Kosovo.
References:
1.Davidson’s Principles & Practice of Medicine 21st edition.
2. Kumar and Clarks Clinical Medicine Eighth Edition.
3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4435650/
4. https://www.medicalnewstoday.com/articles/318472.php
5. https://www.idf.org/aboutdiabetes/what-is-diabetes/facts-figures.html
6 . https://www.who.int/health-topics/diabetes
7. https://www.who.int/health-topics/cancer#tab=overview
9.https://www.sciencedaily.com/releases/2019/08/190825075932.htm
