"What we measured was a massive change in heart lipid composition," Gross says. "In part, it confirms what science has come to recognize--mitochondria are quite dynamic and change shape in response to nutritional and hormonal cues. But we are the first to report that mitochondria essentially remodel their own membranes, and thereby their physical properties, by dynamically altering their use of phospholipids."

A phospholipid decrease of the magnitude reported is all the more surprising because phospholipids comprise essential components of all cellular membranes and have previously been thought to be preserved except in cases of extreme starvation.

The researchers' data also reveal that after feeding resumes, the phospholipid levels in heart muscle cells rise back to normal levels, indicating that mitochondria readily rebuild their membranes.

During this recovery period, another class of lipid, triglyceride, a common source of energy for many types of cells, peaks high above its normal level in heart muscle cells. "The rise of triglyceride isn't easily explained by nutritional conditions, because after feeding resumes, the heart shouldn't need to increase its levels of fats. It's as if the heart retains a memory of deprivation and doesn't want to get caught unprepared again," Gross says.

The next step for the research team will be to study the changes in shape and structure of mitochondria and to relate these to changes to lipid metabolism.

The response by heart mitochondria might lend a partial explanation to a pattern discerned in studies of ischemic heart patients, who have restricted blood flow to the heart.

"While we have to be careful in drawing definitive parallels between mouse lipid dynamics and human lipid dynamics, it is interesting to note that the majority of sudden death in ischemic heart patients occurs in the early morning hours when people have typically had a long fa
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Contact: Gwen Ericson
ericsong@wustl.edu
314-286-0141
Washington University School of Medicine
19-Nov-2004