Otago University researchers, led by Dr Rajesh Katare, a senior lecturer in the Otago physiology department, have discovered why heart disease is the leading killer of people with diabetes.
It had been estimated in the United States that cardiovascular complications resulted in the death of at least 60% of people with diabetes.
The Otago breakthrough finding opened the way for potential new treatments to combat the disease in diabetic patients by targeting a key protein in diabetic heart cells, called Beclin-1, the researchers say.
The Ministry of Health says more than 240,000 New Zealanders have been diagnosed with diabetes, mostly type 2, but it is believed another 100,000 people also have it but do not know.
''Given that the growing diabetes epidemic is set to create major global economic and social costs in coming decades, it is very exciting to have opened up a new research avenue that could greatly decrease the disease's burden,'' Dr Katare said.
Why diabetes proved so damaging to heart health had long remained a mystery, but the Otago study, published in the International Journal of Cardiology, identified harmful molecular changes in the cells of diabetic hearts that began before cardiovascular symptoms even appear.
Using a mouse model for type-2 diabetes, the most common form of diabetes, the researchers found that a normal cell process called autophagy was not well controlled in diabetic hearts.
Autophagy normally involves controlled digestion of damaged organelles within a cell.
But researchers found that a marked increase in autophagy led to progressive loss of cardiac cells.
This would cause cardiac dysfunction to develop, with heart failure ensuing, researchers said.
Otago researchers also identified that diabetes increased autophagy through activation of the Beclin-1 protein.
And this protein presented ''an extremely promising target for new treatments of diabetes-related cardiac disease'', he said.
The research ''makes me feel very proud'', and its potential for developing a new blood marker to indirectly monitor Beclin-1 levels was ''very exciting''.
Indian-born, Dr Katare said he had been partly inspired to undertake research in this field by the sudden death of his father, who had diabetes, in 2008.
''When you start doing the research you always want to save as many people [as you can],'' he said in an interview.
He was optimistic about future research prospects in this field, including finding a non-invasive, accurate way of determining Beclin-1 activity levels in the heart, by analysing levels of a microRNA, a small molecule, in the human bloodstream.
Doctors and patients would benefit from doctors being able to determine levels of the protein in the diabetic heart, and this could help provide early warning of heart health risks, and could help doctors refine treatment options, he said.
The Otago team was able to confirm its laboratory-based results about autophagy by collaborating with cardiothoracic surgeons at Dunedin Hospital to collect and study heart tissue samples from coronary bypass patients.
The researchers matched around 35 such diabetic patients with comparable non-diabetic ones. Analysis revealed markedly increased autophagy in the diabetic patients' heart tissues compared with the non-diabetic ones.
