06/25/2009 - A latest study has revealed how a certain category of diabetes drugs can actually increase the risk of heart failure. The class of drugs under study were thiazolidinediones (TZDs).

TZDs linked to heart failure

Thiazolidinediones (TZDs) have been a topic of controversy since 2007 when an examination of Avandia (rosiglitazone), a TZD made by GlaxoSmithKline, showed that patients consuming it have a higher probability of getting affected by a heart attack.

Statistics have also revealed that TZDs are associated with heart failure. The consumption of this class of drugs leads to a condition wherein the heart is not able to pump sufficient blood throughout the body.

Clay Semenkovich, an endocrinologist at the Washington University School of Medicine in St Louis, Missouri, was quoted as saying, “We already knew if you had heart failure you probably should not be taking these drugs, but this paper provides an additional explanation why.”

One of the important reasons why TZDs are harmful for the heart is that they activate a group of molecules named as Peroxisome Proliferator-Activated Receptors (PPAR). PPARs are a group of proteins that help in regulating the expression of genes.

Study details

At the commencement of the study, the main purpose of the authors was to identify what actually happens when the heart muscles enlarge. They did not focus on the diabetes drugs.

Wilhelm Krek, a cancer biologist at the Swiss Federal Institute of Technology in Zurich, said, “If a cancer grows, it outstrips its nutrient and oxygen supply.”

Researchers believed that a similar sort of mechanism might be taking place in the body when the heart expands in case of a heart attack or during chronic high blood pressure.

Due to the increase in its size, the heart is primarily able to pump more blood but this can eventually make it weak. The enlarged hearts need to work harder to get oxygen. Consequently, it starts burning glucose instead of fat. Because of the accumulation of fat, heart cells ultimately weaken and then eventually die.

It was found that PPAR might aid in this dilapidated condition of the heart, but it was discovered that increased levels of PPAR in heart tissues also caused the conditions that led to heart failure.

When the researchers experimented on the heart cells of the mice, they found out that elimination of PPAR inhibited the accumulation of fat in the heart cells and they did not collapse.

The current study has been published in the June issue of Cell Metabolism.

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