Study Shows Link Between Pancreatic Hormone And Heart Damage

Study Shows Link Between Pancreatic Hormone And Heart Damage

UC Davis researchers have found that amylin, a pancreatic hormone, is linked with severe heart failure in obese and diabetic patients. The study conducted on animal model revealed that amylin, the hormone that produces satiety after eating, accumulates in the heart muscle and contributes to major cardiac dysfunction.

Amylin is an amyloidogenic peptide co-secreted with insulin by pancreatic beta cells and it s overexpression seems to occur in the prediabetic stage. Normally, amylin circulates in the blood  with insulin, the hormone that regulates glycemia, and in relatively small amounts.

The study, led by Sanda Despa, an  assistant professor of pharmacology at UC Davis, emphasises that obesity and type 2 diabetes mellitus are linked to cardiomyopathy, independent of hypertension and coronary artery disease. As heart failure is the major cause of death in obese and cardiac people, reducing the level of amylin hormone could not only improve cardiac function, but also prevent potential complications. Studies conducted on both normal and failing  donated hearts, showed that, in thin people, there was no or little amylin buildup. However, in obese and diabetic patients, there has been found extensive deposits of amylin organized in fibers formed of 10 or 20 oligomers. Moreover, accumulation of amylin has also been found in overweight people but not obese people. It is worth mentioning that amylin accumulates not only in the heart muscle, but also in pancreas. The overexpression of amylin is responsible for beta cells death and progression to type 2 diabetes mellitus. Similar buildups have been found in kidneys in type 2 diabetes mellitus patients, which confirms the fact that amylin accumulates in other organs, besides heart muscle an pancreas.

Scientists found that amylin oligomers link to the membrane of the heart muscle cells in charge of heart beats. Consequently, the permeability for calcium ions increases and eventually the myocites die. Florin Despa,an assistant professor of pharmacology at UC Davis and senior author of the study, is optimistic about this new discovery. He thinks that substances that prevent amylin from shaping into oligomers could reduce heart failure. He also said that the role of amylin in cardiac dysfunction has been overlooked because this hormone circulates in small amounts in blood. Another reason was that the form of amylin expressed by rats used in experiments is different from the one expressed by humans.

In order to detect amylin oligomers in human and rat heart tissues, the researchers used immunohistochemistry, immunofluorescence and Western blot. Cardiac dysfunction in the rats was assessed by investigating the function of  normal myocites  and those myocites deteriorated by the accumulation of amylin.