LA JOLLA, Calif., November 1, 2010 One of the many advantages of maintaining a normal body weight is having healthy fat, which in turn supports a healthy heart. Fat tissue is increasingly seen as more than just a storage depot it's also an active secretory organ that normally produces high levels of a cardioprotective hormone called adiponectin. How adiponectin protects the hearts of healthy people has long been a mystery, and now a team led by Barbara Ranscht, Ph.D. and Pilar Ruiz-Lozano, Ph.D. at Sanford-Burnham Medical Research Institute (Sanford-Burnham) reveals that the protein T-cadherin is the receptor that anchors adiponectin to heart cells. This new study, published November 1 in The Journal of Clinical Investigation, helps answer the longstanding question about how adiponectin prevents stress-induced damage in 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," explained 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."
Dr. Ranscht's laboratory previously studied T-cadherin for its role in brain development and cancer, and had noted T-cadherin's abundant expression in the heart when discovering this molecule in the early nineties. The best way to determine T-cadherin's role in heart protection is to see what happens when the protein is missing, so Dr. Ranscht and colleagues engineered mice that lacked T-cadherin and looked at their hearts. They found that adiponectin was no longer able to bind to heart tissue, leaving more hormone flowing in the bloodstream. The researchers then exposed T-cadherin-deficient animals to cardiac stress by restricting
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Sanford-Burnham Medical Research Institute