Without a doubt, it could at first glance be taken as an April Fool’s Joke. Yet this report, which a team under Barbara Ranscht and Pilar Ruiz-Lozano at the U.S. Sanford-Burnham Medical Research Institute has now published, is based on reliable biochemical knowledge and is considered the first work of its kind. In fact, researchers have suspected for some time that the hormone, adiponectin (APN), stored in the body fat, could protect the heart in healthy people. This phenomenon nevertheless remained until now quite a mystery – no one knew the exact cause, nor the mechanisms for the protective effect. Furthermore, experimental studies were missing, which might have been able to provide evidence about the relevant protective function.
Now however it seems clear: The fat of Homo sapiens sapiens makes use of a tiny protein that allows the species to avert cardiac-related death in stressful situations. T-cadherin, as it is specifically known, acts – according to the results now published by the American researchers – as a sort of molecular anchor on the surface of the heart muscle. In this way the protein is able to bind adiponectin, which is released by human fat into the blood. There are those who will at first be happy about that. Among 35-year-old men, every second one is overweight; among women, the same situation applies for 55 year-olds and older. About 15 percent of children and young people between 5 and 17 years of age are overweight, seven percent are obese . Meanwhile, more than half of the German population carries too much weight, the trend being an increasing one. No longer a problem, thanks to APN?
Those who, because of the U.S. publication, as cardiologists fear having their own heart attack, can breathe easier. Because, according to Ranscht, fat is not always one and the same problem. Nobody in the future will be greatly challenging the dogma of “the normal BMI“ itself but perhaps – and already in some small way – view of fats, the study suggests. This emerges in particular in animal studies, in which mice, whose production of T-cadherin was blocked, weren’t able to use adiponectin as a protective shield for their hearts. In order to demonstrate the protective effect of this combination, the U.S. Researchers exposed the animals to extreme stress situations. Mice lacking adiponectin on their heart muscle-tissue surface suffered sudden death. Why the interaction between fat hormone and receptor protein works at all is still not fully understood. Apparently, the molecules set a biochemical cascade in action in which, according to the study, the AMP-activated protein kinase AMPK (a regulator of cell energy) is involved. Adiponectin possibly serves in the overall mechanism as a link member and as a molecular switch at the same time, by conveying an activation signal from T-cadherin to AMPK.
Fit for fat?
Advising one’s patients to eat to the max in order to increase body fat mass would still be inappropriate, because the irony is that – of all things – the overweight, despite conspicuous fat reserves, produce “much less adiponectin than people of normal weight”, Rantsch informs. Athletes in turn produce even more APN than couch potatoes, which is an observation that current heart attack prevention measures support.
But why do heart attacks keep occurring to competitive athletes? The two Americans have a simple explanation for that: the sudden cardiac deaths of athletes are mostly due to hypertrophic cardiomyopathy and are thus of a hereditary nature. Biochemists know that a total of ten genes which encode for the so-called cardiac Sarcomere are considered to be the triggerr of the life-threatening disease, affecting not only competitive athletes.The protective action of fat simply never comes in to oppose it, speculates Rantsch.