It has been known that diabetes raises the risk of heart failure. Researchers recently determined the cellular link contributing to the increased risk.
Diabetic patients are at a significantly higher risk of developing heart failure. Studies have shown that men with diabetes are 2.4 times more likely and women five times more likely to suffer heart failure compared to non-diabetics. Also, the primary cause of death for diabetes patients is cardiovascular disorders such as heart failure, heart attack and coronary artery disease. So, what is the link between diabetes and heart failure?
Heart failure is a serious condition which can be fatal. It occurs when the heart is unable to pump blood around the body properly and cannot pump enough blood to meet the body’s needs. Conditions such as narrowed arteries (coronary artery disease) or high blood pressure can gradually cause the heart to become too weak or stiff to fill and pump efficiently, leading to heart failure. Patients with heart failure experience symptoms such as fatigue, swelling in the legs and shortness of breath.
Despite the increasing number of people affected by diabetes worldwide, it remains unclear why diabetes can lead to heart failure. The discovery of abnormalities at a cellular level that contributes to heart failure in diabetics is important in providing potential medications to help treat and possibly prevent heart failure in diabetes patients.
A study at the cellular level
A recent study published in JCI Insight by researchers in the United States investigated at a cellular level how diabetes can cause heart failure. They looked at the impact a molecule called methylglyoxal had on heart tissue from three different groups of people, people without heart failure, people with heart failure who had diabetes and people with heart failure who did not have diabetes.
People with diabetes are unable to clear out cell waste products as efficiently
During the process of transforming food into chemical energy, various waste products are produced. One of these waste products is methylglyoxal. Typically, the body can efficiently clear out this waste product. However, diabetics are unable to clear it out as efficiently, resulting in an accumulation of methylglyoxal, which attaches to building blocks of proteins. This, in turn, affects protein function in cells.
Waste product methylglyoxal affect microscopic structures that allow the heart to contract
The results of the study showed that methylglyoxal modifies myofilaments, which are microscopic lattice-like structures found in the heart that cause the heart muscle cells to contract and pump blood around the body. Methylglyoxal modified microfilaments in heart tissue of patients with diabetes and heart failure compared to patients who either didn’t have heart failure or who had heart failure without diabetes.
The study also showed that the modifications caused by this molecule weakened the heart muscle cells by interfering with processes within the cell. As methylglyoxal builds up in the cells of diabetic patients, it causes myofilaments to not be able to contract as well. This can lead to heart failure as the heart is unable to pump blood efficiently.
Findings could lead to new drug treatments
These findings suggest that the effects of methylglyoxal are a key component in the link between diabetes and heart failure. Therefore, the development of a new drug which counters the effects of methylglyoxal could provide a possible treatment or even prevention for the growing population of diabetic patients who are at risk of heart failure.
Written by Lacey Hizartzidis, PhD
- Papadaki M, Holewinski RJ, Previs SB, Martin TG, Stachowski MJ, Li A, BlairCA, Moravec CS, Van Eyk JE, Campbell KS, Warshaw DM, Kirk JA. Diabetes with heartfailure increases methylglyoxal modifications in the sarcomere, which inhibit function. JCI Insight. 2018 Oct 18;3(20). pii: 121264. doi:10.1172/jci.insight.121264.
- Why does diabetes cause heart failure? EurekAlert website https://www.eurekalert.org/pub_releases/2018-10/luhs-wdd101118.php. Accessed January 10, 2019.