Regulation of pancreatic -cells may be key to improving heart attack recovery

Mutations in the gene for a protein involved in repairing damaged protein surfaces in the pancreas have been found to be associated with a higher risk of heart attack. A study led by researchers at Karolinska Institutet in Sweden indicates that bioactive molecules released by pancreatic beta cells and secreted by beta cell receives these signals to regulate the blood sugar level in the target organs and improve the tolerance of heart attack patients. The study is published in the scientific journal Cell Reports.

Years of research have led to the identification of what are called glycoproteins e.g. insulin-1 and insulin-2 which are responsible for producing glucose the energy molecule of the body. After the origins of insulin-1 and insulin-2 gene mutations it was found that the amount of glucose produced by beta cells increased considerably if the mutation is found and affects the cell surface proteins called lactate dehydrullase 2 and lactate transporter 1.

The research group led by medical student Terje Aarsen from the Department of Womens and Childrens Health at Karolinska Institutet and Partnerships for Precision Medicine at the Karolinska Institutet focussed on complications of the chest wall without any clear causes so it was not possible to have established a causal role of the mutations in blood (DoC). The researchers therefore set out to find ways of monitoring the microcirculation of blood glucose levels in patients with heart attacks to improve their recovery.

Mutations of glycoproteins are found in up to one per cent of all patients with heart attacks and one per cent with non-hypertensive people. The magnitude of the effect that such mutations have on the microcirculation of blood glucose may not be sufficiently large to see clearly in a graph.

But it is not the size of the data sets the diversity of the population afflicted by heart attacks or differences in the statistical methods that are the major issues say the researchers. The biggest problem is that the molecular pathways for glysee binding are regulated by variations of gene expression. The researchers represent this as causing differences in gene expression not in genes themselves as previously assumed.

Moreover the translocations of glycoproteins only affect the beta cells and not the liver or pancreas. Some genes expressed in other tissues have also been associated with the development of heart attacks.