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DISRUPTED FAT CELL SIGNALING IN OBESE MICE LINKED TO INCREASED CELL DEATH IN ENLARGED HEARTS

Johns Hopkins Medicine
Office of Corporate Communications

Media contact: David March
410-955-1534; dmarch1@jhmi.edu

March 8, 2005

DISRUPTED FAT CELL SIGNALING IN OBESE MICE LINKED TO INCREASED CELL DEATH IN ENLARGED HEARTS

Disrupted fat cell signaling in obese mice has been linked to increased cell death, or apoptosis, in enlarged hearts.  According to the Johns Hopkins researchers who led the study, the research is needed to understand how obesity contributes to enlarged hearts (hypertrophy), subsequent heart failure and increased risk of death.

"The work also suggests a biological route for potential therapies that could block or reverse obesity's harmful effects on the heart," says lead investigator and cardiologist Lili Barouch, M.D., an assistant professor at The Johns Hopkins University School of Medicine and its Heart Institute.

The researchers studied heart muscle enlargement and cell death in more than 20 male and female mice, some normal and others inbred for obesity due to changes in the amount and function of the hormone leptin.  Some mice were leptin deficient, while others had nonworking leptin receptors.  Made by fat cells, leptin regulates appetite and energy balance. Normally, greater quantities of leptin are released from fat cells when an animal is "full," as a signal to stop eating, but the signal is blocked in
obesity.  Comparison of heart tissue samples from obese mice and normal mice showed that when leptin signaling was disrupted, the hearts became enlarged and apoptosis increased by more than 10 times what occurs in normal tissue.  When leptin levels and function were restored, apoptosis
activity returned to nearly normal levels.

Cardiac myocyte apoptosis is associated with left ventricular hypertrophy in murine models of obesity. Lili Barouch, Daquing Gao, Lei Chen, Shakil Khan, Shubha Raju, Koenraad Vandegaer, Christopher O'Donnell, Dan Berkowitz, Chiming Wei, and  Joshua Hare.

(NEWS TIPS FROM THE 54th ANNUAL SCIENTIFIC SESSIONS OF THE AMERICAN COLLEGE OF CARDIOLOGY (ACC), MARCH 6-9, 2005, ORLANDO, FLA.  Abstract presentation #860-4, Room 230-B, Orange County Convention Center.)

 

 


 

 

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