obesity neurons identified in fruit flies

Caltech scientists have isolated two groups of neurons in fruit fly brains that are capable of sensing and manipulating the fly's fat stores - making these flies a potential useful model for the study of obesity in humans.
The findings are published in the August 13 issue of the journal Neuron.
The researchers manipulated the neural activity in fruit fly brains using transgenic techniques and discovered that, "just as in mammals, fly fat-store levels are measured and controlled by specific neurons in the brain," says Caltech postdoctoral scholar Bader Al-Anzi, the Neuron paper's first author. "Silencing these neurons created obese flies, while overactivating them produced lean flies."
Our brains are given information about our fat stores via hormones such as insulin and leptin - and respond to the signals by inducing changes in food intake and metabolism to maintain a stable body weight. The researchers discovered that similar behavioral and metabolic changes occurred in the fruit flies - though the changes observed depended upon which of the two sets of neurons was silenced.
For example, silencing one group of neurons led to an increase in food intake, a decrease in metabolism, and an increase in the synthesis of fatty acids (the building blocks of fat). Silencing the other group led to a similar decrease in metabolism and increase in fatty-acid synthesis, as well as to a defect in the flies' ability to utilize their fat stores.
Increasing activity in either of the groups of neurons, on the other hand, resulted in depletion of fat stores by increasing the flies' metabolism and decreasing their synthesis of fatty acids.
The next step is to "see exactly how neurons regulate fat storage, and how the two different groups of neurons identified in this study work," says Kai Zinn, professor of biology at Caltech, who led the research group. "They clearly regulate fat storage using different mechanisms."
For additional information, see the official release: http://media.caltech.edu/press_releases/13285



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