Disabling enzyme allows mice to gorge without becoming obese, new s...(he disparity in weight gain became clear...)

The researchers noted that the missing AdPLA did not change the number of fat cells, but simply kept the cells from accumulating excess fat.

The researchers also studied whether loss of AdPLA could prevent genetic obesity in mice. They compared mice that lacked leptin, the hormone that signals when the body is full, with mice that lacked both AdPLA and leptin. Leptin-deficient mice are voracious eaters, typically consuming two to three times more food per day than normal mice, and they rapidly develop obesity.

In this study, leptin-deficient mice ate an average of 5 grams of food per day, while mice that lacked both AdPLA and leptin ate 7.5 grams. Typically, normal mice will eat only 2-3 grams per day. By 17 weeks of age, the leptin-deficient mice were already hitting the scales at 75 grams. In comparison, mice that lacked both AdPLA and leptin weighed just under 35 grams.

The researchers found that levels of AdPLA increase after eating to block fat breakdown, and decrease with fasting to allow fat breakdown to proceed efficiently. They also found that levels of AdPLA are higher in obese mice.

"This means that local signals in fat tissue allow fat cells to directly regulate fuel provision for the body, which changes our fundamental understanding of how the body regulates fat breakdown," said Ahmadian, another study co-lead author. "We found that mice deficient in AdPLA expend more energy than normal mice, and they also burn more fat directly within fat cells."

Before this paper, the assumption had been that the major players in controlling fat metabolism and body weight were endocrine factors, primarily hormones that are secreted by di
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