Researchers here demonstrate the degree to which fat tissue is involved in the progression from hypertension to heart failure, achieving this result by finding a way to sabotage one of the linking mechanisms. Removing a specific gene, ATGL, greatly reduces heart failure in mouse models of the condition. ATGL appears to play an important mediating role in the way in which fat tissue produces altered lipid levels in an aged, dysfunctional heart, and those lipid changes in turn accelerate the decline into heart failure. The full paper is open access, and worth looking over if the topic interests you. It should go without saying that there is already a mountain of research to demonstrate that excess fat tissue is a bad thing: this adds one more item to that lengthy list.
Heart failure is a chronic disease that should not be underestimated. Between one and two thirds of patients with heart failure die of the disease within five years. While researching the molecular causes of heart failure and new ways to treat it, researchers found that changes in adipose (fat) tissue lipid metabolism affect disease development. "We were able to show that the lipid composition of the heart is altered by non-cardiac body fat, and that these changes are likely to affect heart function."
For some time, researchers have suspected that the impact of body fat on heart function also exists on a molecular level. One of the key processes involved is the release of fatty acids from adipose tissue. In order to gain a better understanding of this process, the researchers used an animal model, which allowed them to interfere with the lipid metabolism, and to knock out the gene responsible for the relevant enzyme, adipose triglyceride lipase (ATGL). This resulted in all treated mice developing near-complete protection against heart failure. As part of this study, the researchers also analyzed blood samples from patients with and without heart failure. Some aspects of the changes observed in the lipid composition of blood samples were comparable to those observed in the animal model.
The researchers are now planning to transfer these results into clinical practice. In doing so, they will be guided by one central question: how might a drug-based treatment target the gene responsible for the release of fatty acids and the enzyme ATGL, and how might it do so exclusively in adipose tissue? The researchers are also planning to conduct further analyses of patient samples to confirm their results, and are working to determine the role of adipose tissue in patients with heart failure within the clinical setting. "For patients, this means that we should be starting to pay greater attention to adipose tissue when making diagnostic and treatment decisions, even when our primary aim is to treat heart disease."