New master switch found in the brain that regulates appetite and re...(ten do not have periods.) Controllin...)

"Controlling appetite and reproduction together provides a big evolutionary advantage," Montminy says. "If there is no food, the brain believes the body should not reproduce because without body fat, a baby's growth in the womb could be stunted, and without food to replenish the body's energy reserves, there will be nothing to feed the offspring."

"Leptin works remarkably well to give the brain a good indication of how much food has been eaten; 99.9 percent of the time it balances food intake with energy use," he says. "The problem is that no machine works 100 percent of the time, and that slight bit of inefficiency can lead to extra body weight."

Obesity results when the brain becomes "deaf" to the leptin signal, so one goal of Montminy's research is to "try to make a way to make sure the brain signals are being heard." But to do that, he and his research team first have to understand all of the signals involved in the satiety pathway.

Through years of research, they have uncovered a family of genes that act as energy switches, turning other genes on or off. One gene, TORC2, acts like a fasting switch that flips on the production of glucose in the liver when blood glucose levels run low, usually during sleep. During the day, the hormone insulin normally shuts down TORC2, ensuring that blood sugar levels don't rise too high. Problems along the pathway, however, can help lead to diabetes.

In this study, Altarejos looked at the function of TORC1, which she knew was produced in the brain unlike TORC2 and TORC3 but didn't know what its function was. To do this, she created mice that lacked one or both copies of the TORC1 gene the first such "knock-out" mice to be developed.

Mice born without TORC1 looked fine at birth, but at about eight weeks, they began to gain weight and became persistently obese in adulthood, with two to three times as much adipose fat as normal mice, and they also became
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