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A different path to fat-related heart disease
Date:1/18/2011

levels of triglycerides, heart-damaging fats commonly associated with obesity and type 2 diabetes in humans. The disruption in cell membrane fat synthesis and consequent triglyceride fat accumulation added up to heart problems for flies short on PE-producing enzymes. Compared to their genetically normal counterparts, they were especially prone to cardiac arrest under stress and other heart problems.

Since overactive SREBP seems to be the cause of heart disease in this system, can it be targeted to reduce heart disease? The researchers addressed this question by inhibiting SREBP or its fat-synthesizing target genes through genetic manipulation. In doing so, they were able to restore fat balance and rescue PE-deficient flies from heart malfunction. These beneficial effects were also achieved by reducing SREBP in just the heart, rather than the whole fly. As a result, the flies were still obese, but their hearts functioned normally. These findings further underscore the importance of SREBP in excess fat-related heart diseases, like lipotoxic cardiomyopathy.

"Here we identified a new metabolic pathway that exhibits striking similarities to obesity- and diabetes-related heart failure in humans," explained Dr. Bodmer, professor and director of the development and aging program at Sanford-Burnham and senior author of the study. "This information might now allow us to interfere with the toxic effects of high fat in the heart by directly manipulating these genes in the heart muscle."


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Contact: Josh Baxt
jbaxt@sanfordburnham.org
858-795-5236
Sanford-Burnham Medical Research Institute
Source:Eurekalert

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