SYDNEY – A groundbreaking study has demonstrated that Type 2 diabetes directly alters the heart’s structure and its energy systems. The research provides crucial insights into why diabetic patients face a significantly higher risk of heart failure, even in the absence of arterial blockages or hypertension.
Conducted by researchers at the University of Sydney and published on August 4th in the journal EMBO Molecular Medicine, the study was also highlighted by EurekAlert!. For decades, clinicians have observed that diabetes silently damages the body over time, leading to a higher incidence of heart failure. However, the precise biological mechanisms behind this strong correlation have remained elusive.
Now, by analyzing donated human heart tissue, Dr. Benjamin Hunter and Dr. Sean Lal from the University of Sydney’s Faculty of Medicine and Health have uncovered the direct molecular impact of diabetes on the heart muscle.
Uncovering the Molecular Fingerprint of Diabetes on the Heart
The research team examined heart tissues from organ transplant recipients and healthy donors. Their analysis revealed that diabetes causes distinct molecular changes in heart cells and muscle structure, particularly in patients with ischemic cardiomyopathy—the most common cause of heart failure.
The findings show that diabetes fundamentally alters how the heart produces energy and maintains its structure under stress. Using advanced microscopy techniques, the researchers observed direct physical consequences: a buildup of stiff, fibrous tissue within the heart muscle.
The study explains that elevated glucose levels can cause proteins within the heart muscle to stiffen—a process known as glycation. Over time, even minor changes accumulate, progressively remodeling the heart in ways that are difficult to detect until symptoms of heart failure appear.
Getting to the Heart of the Problem
The study establishes that diabetes is not merely a co-occurring condition with heart disease; it actively worsens heart failure by disrupting key biological processes and microscopically reshaping the heart tissue.
“The metabolic impact of diabetes on the human heart has not been fully understood,” explained Dr. Hunter. “A healthy heart primarily uses fats, along with glucose and ketones, as fuel. While it was known that glucose uptake increases in heart failure, diabetes simultaneously reduces the sensitivity of glucose transporters—proteins that shuttle glucose in and out of cells—to insulin in heart muscle cells.”
The researchers observed that diabetes exacerbates the molecular signatures of heart failure in advanced-stage cardiac patients. It places additional stress on the mitochondria, the energy-producing powerhouses of cells. Furthermore, they noted a decline in the production of proteins essential for heart muscle contraction and calcium handling in patients with both diabetes and ischemic heart disease. This, combined with the accumulation of fibrous tissue, severely compromises the heart’s ability to pump blood effectively.
Dr. Hunter added that RNA sequencing confirmed that many of these protein-level changes were also reflected at the genetic level, particularly in pathways related to energy metabolism and tissue structure, thereby reinforcing their observations.
“This research connects heart disease and diabetes in previously undiscovered ways in humans,” said Dr. Lal. “It provides new insights into potential therapeutic strategies that could benefit millions of people in Australia and worldwide.”
The findings underscore the critical importance of early and proactive cardiovascular monitoring for individuals with diabetes, highlighting that the damage begins long before clinical symptoms emerge.
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