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Fatheads: How neurons protect themselves against excess fat
Date:4/8/2013

he two types of mice as long as they had ready access to food, Wolfgang says. But when food was taken away overnight, so that the mice's cells would start to break down their fat stores and release fat molecules into the bloodstream for use as energy, ACOT7's role began to emerge. While the normal fasting mice were merely hungry, the mice lacking ACOT7 had poor coordination, a sign of neurodegeneration. More differences emerged when the researchers dissected the mice; most strikingly, the livers of mice missing ACOT7 were "stark white" with excess fat, Wolfgang says.

Wolfgang cautions that his group's results are not quite a smoking gun for ACOT7's involvement in human neurological disease, but says they add to existing circumstantial evidence pointing in that direction. He notes that a special diet that changes the levels of fats and sugars in the bloodstream the so-called ketogenic diet can prevent seizures in epileptics; in addition, one study found that patients with epilepsy have less of the ACOT7 enzyme than healthy people.

"We think ACOT7's purpose is to protect neurons from toxicity and death by allowing excess fat to escape the cells," Ellis says. "Our next step will be to see whether this enzyme does indeed play a role in human neurological disease."


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Contact: Shawna Williams
shawna@jhmi.edu
410-955-8236
Johns Hopkins Medicine
Source:Eurekalert

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