- In donated left ventricle tissue, people with ischaemic cardiomyopathy and diabetes showed a distinct molecular pattern linked to poorer energy handling and more scarring compared with similar heart failure without diabetes.
- The strongest signals were around mitochondrial energy production, oxidative stress and fibrosis, with changes in proteins involved in fat handling too.
- This is end stage heart failure tissue, so it cannot prove diabetes causes these changes early on, but it highlights pathways that could help explain why outcomes are worse when both conditions overlap.
People with type 2 diabetes are more likely to develop heart failure, but the reasons are not fully explained by cholesterol, blood pressure and blocked arteries alone.
A new study adds another piece to the puzzle by looking directly inside human heart muscle.
Researchers in Sydney analysed samples of left ventricular myocardium taken from people with end stage heart failure, including those with ischaemic cardiomyopathy, and compared groups with and without diabetes against healthy age matched donor hearts.
They used a “multi omics” approach, combining protein, metabolite and lipid profiling with gene expression and high resolution microscopy to see what was happening inside the cells.
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The clearest finding was that the combination of ischaemic cardiomyopathy and diabetes came with stronger signs of disrupted energy production and tissue remodelling than heart failure without diabetes.
Markers linked to oxidative phosphorylation and oxidative stress appeared more affected, and there were signals consistent with more myofibrosis, meaning more fibrous, stiff tissue building up in the heart muscle.
The team also reported broad changes in pathways related to fat handling, including reduced levels of proteins involved in fatty acid transport and oxidation in the diabetes plus ischaemic cardiomyopathy group compared with donors.
Interestingly, the authors note the picture is not simply “fat use is broken”.
They also saw patterns involving acylcarnitines and other fuel pathways which suggest the heart’s fuel mix may be shifting in a more complex way than older models assume.
What does this mean for people living with type 2 diabetes?
It supports the idea that diabetes can “confound” heart failure biology, pushing the heart further towards an energy stressed, fibrotic state.
That could help explain why heart failure risk and outcomes tend to be worse when diabetes is present.
There are important limits.
These samples came from people with very advanced disease, many receiving transplants, so we cannot assume the same changes happen early in type 2 diabetes or in everyone with diabetes.
This kind of study also cannot prove cause and effect. Still, it gives researchers more specific targets, particularly mitochondrial function and fibrosis pathways, to investigate in future treatments and earlier disease stages
