It's about time

Research Updates
 
Every year, National Diabetes Week raises awareness of diabetes and how it affects Australians. It’s about time we did a better job of detecting all types of diabetes.

Around 1.7 million Australians currently live with diabetes. Every day, a further 280 Australians develop diabetes – that’s one person every 5 minutes. The picture is just as dire globally, with the International Diabetes Federation estimating that 415 million adults were living with diabetes worldwide in 2015. This number is likely to more than double in the next 20 years.

Diabetes is one of the main risk factors for developing heart disease. In fact, people living with diabetes are twice as likely to develop heart disease as those without diabetes.

That’s why the HRI is conducting several research projects around detection, prevention and treatment, that are relevant to both diabetes and heart disease. 

Discovering better diagnostic markers, predictors, and therapies for cardiometabolic disease

Obesity-driven metabolic disease such as insulin resistance, diabetes and fatty liver disease are the major drivers of atherosclerotic cardiovascular disease in the modern era, while obesity-driven type 2 diabetes has dramatically increased in prevalence in Australia and other Western countries in the last few decades.

One of the cornerstones of treatment of type 2 diabetes is early intervention. The Cardiometabolic Disease Group, led by Dr John O’Sullivan, has discovered a new molecule that independently predicts diabetes 12 years before diagnosis. This discovery has huge clinical potential to facilitate intervention well before overt onset of diabetes and its complications, such as heart disease. By detailing the entire pathway-controlling levels of this molecule, the Group will be able to more thoroughly assess its therapeutic potential and determine if this pathway can be used to treat fatty liver disease and/or type 2 diabetes.

Treating the complications of type-2 diabetes

Heart disease is the leading cause of morbidity and mortality in diabetes, accounting for up to 80 percent of premature excess mortality. The Translational and Bioengineering Group, led by Associate Professor Martin Ng, has strong interests in unravelling the fundamental reasons why patients with diabetes suffer from accelerated vascular disease and to develop new treatments. In pioneering work, they found that high glucose levels in diabetes directly interfere with the regulation of a protein called Thioredoxin Interacting Protein, or TXNIP, one of the most glucose-sensitive genes in the entire human genome. By preventing high glucose-mediated interference with TXNIP, the Group has been able to strikingly rescue the vascular damage of diabetes, with important implications for the development of new, more effective therapies. The Group has worked toward developing TXNIP as a therapeutic target for the vascular complications of diabetes as well as begun investigating whether there is a link between TXNIP and accelerated atherosclerosis in diabetes.

Investigating TRAIL, a factor in the development of vascular disease

Diabetics are more likely to develop cardiovascular diseases, particularly peripheral artery disease (PAD) – conditions where narrowed arteries reduce blood flow to the heart and limbs. This is a major risk factor for lower-limb amputation. The Vascular Complications Group, led by Dr Mary Kavurma, has identified a new player in the development of vascular disease: TNF-related apoptosis-inducing ligand, otherwise known as TRAIL. The Group has shown that TRAIL stimulates blood vessel growth in ischaemic PAD, highlighting an exciting and novel therapeutic possibility in patients where current treatments have no benefit. The Group has also examined the effect of high insulin levels on vascular smooth muscle cells (the main structural cells in the blood vessel wall) and published their findings in the Journal of Diabetes. They showed that acute insulin exposure to these cells stimulated TRAIL expression and cell growth, yet chronic insulin exposure repressed TRAIL and promoted cell death. These findings are significant since insulin’s differential regulation of TRAIL-dependent cell growth and/or death may have important consequences for insulin’s effect on vascular smooth muscle cells at different stages of diabetes-associated heart disease. 

 

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