Body Fat Sensor Slows Heart Disease

New research has disclosed that a cellular fat sensor in the body slows the development of lesions that could lead to heart disease and suggests this pathway could be used to develop drugs for heart disease. The findings were reported in the October 17, 2003, issue of Science.

Investigators uncovered a regulatory molecule called PPAR-delta (peroxisome proliferator-activated receptor), which plays an important role in the body's inflammatory response to the beginning phase of atherosclerosis. The PPAR-delta switch cuts heart disease in half by disrupting a cellular signal that controls the inflammatory response. Thus, activation of PPAR-delta reduces inflammation and discourages the growth of atherosclerotic plaques.

"The lesions that cause atherosclerosis are very complex and are aggravated,” said Ronald Evans, chair in molecular and developmental biology at the Salk Institute (La Jolla, CA, USA), who along with colleagues conducted the study. "We believe that PPAR-delta normally acts as a molecular soldier to guard against inflammation and disease. Unfortunately, these good effects are compromised by high-fat diets, poor exercise, infections, and stress.”

Dr. Evans suggests that chemicals regulating the activity of PPAR-delta could form the basis of a new drug to reduce atherosclerosis and therefore be a possible therapy for heart disease.




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