Researchers have confirmed that healthy fat can help protect a person against heart attack.

Healthy fat, which is contrast to obese fat, produces adiponectin, a cardio-protective hormone. Now, researchers at the Sanford-Burnham Medical Research Institute (Sanford-Burnham) have found that a protein T-cadherin is the receptor that anchors adiponectin to heart cells which in turn protects the heart.

“Whereas healthy people usually have high adiponectin levels circulating in their bodies, obese fat is different from healthy fat. Obese fat produces less adiponectin, reflected in lower levels of adiponectin found in serum,” said Dr. Ranscht, professor in Sanford-Burnham’s Tumor Microenvironment Program and senior author of the study.

“Many clinical studies correlate low adiponectin levels with an increased risk for heart disease, stroke and other cardiovascular dysfunctions.” The study may provide researchers a clue on how adiponectin prevents stress-induced damage to the heart.

T-cadherin role in cancer and the development of the brain was previously studied by Dr. Ranscht’s laboratory. The research conducted in the early nineties found an abundance of the protein in the heart while discovering this molecule.

The research team used mice which lacked the protein and then examined the heart to find that the percentage of hormone flowing in the bloodstream. It was found to be higher as the adiponectin was unable to bind the heart tissue. The animals with diminished T-cadherin were exposed to cardiac stress by considerably restricting the blood flow. The mice induced with mutant strain of T-cadherin suffered from damage to the heart and the symptoms were similar to the mice lacking adiponectin.

The researchers attempted a rescue experiment to prove the connection of T-cadhrin and adiponectin in protecting the heart. Inducing adiponectin to the mice deprived of the hormone reversed heart damaged induced by stress. If the protein T-cadherin was necessary for the mediation of adiponectin induced protection a similar rescue would not be possible for the T-cadherin-deficient mice. The researchers had to generate a mouse model which lacked both the receptors and the hormone. The study found that adding adiponectin to the double mutant mice did not help in treating the stress-damaged hearts. This clearly undermines the need of T-cadherin for adiponectin to function in the heart.

According to Dr. Ranscht, tests determining the necessity of T-cadherin for adiponectin’s other beneficial functions in metabolism and inflammation are required. The test should also identify pathways connecting T-cadherin to the activation of AMPK in the heart. “Our work shows that T-cadherin is necessary for adiponectin functions, but we still don’t know how T-cadherin transmits the adiponectin-binding signal into the cell. We are now searching for proteins that might functionally associate with T-cadherin and thus form the molecular link between T-cadherin and AMPK,” he said.