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MAY 19, 2015 by APRIL McCARTHY
Research Finds Appetite Hormones Are Not The Overeating Culprit

For years, scientists have pointed to leptin resistance as a possible cause of obesity. Research led by investigators at the University of Cincinnati (UC) Metabolic Diseases Institute, however, found that leptin action isn't the culprit.


"Restoring leptin action will not be effective at reducing obesity because leptin action is normal as opposed to being impaired in obesity," says assistant professor Diego Perez-Tilve, PhD, who directed the study "Diet-Induced Obese Mice Retain Endogenous Leptin Action" which appeared in the science journal Cell Metabolism on May 14, 2015.

Leptin is a hormone that plays a role in appetite and weight control. It is produced, Perez-Tilve says, when we are well fed, and it signals to the brain that there is ample energy and therefore reduces eating. If you have a lot of leptin circulating, you feel more full and probably eat less.

But obese and overweight individuals often become leptin-resistant -- they have very high levels of it, but it doesn't work. There's a short circuit in their satiety system, and having a certain amount of fat is what causes it.

A premature surge of leptin in newborn mice delivered by underfed mothers results in a change to important brain circuits controlling energy regulation, other researchers reported.

Leptin has been a hormone of interest since 1994, he says, when scientists discovered that a particular strain of obese mouse couldn't produce leptin at all.

"That mouse was very obese because it was hungry all the time. When they treated the mouse withleptin, it stopped eating so much and started losing weight."

Perez-Tilve says scientists were initially puzzled because obese persons have leptin levels far higher than persons of average weight. They theorized that the body was making extra leptin to combat obesity and that the obese patients must therefore need more leptin than persons of average weight to signal the brain to stop eating. However, in human preclinical trials, "giving obese patients more leptin didn't work ... they ate the same and remained obese, so it was concluded that obesity was a state of leptin resistance," he says.

In the UC study, funded by the National Institutes of Health, the team headed by Perez-Tilve took a different approach. They blocked leptin action in both lean and obese mice. The results were that both sets of mice ate more and gained weight to the same extent, proving that "leptin action was not impaired in the obese mouse."

We have evolved to hold on to fat, he says, so if you lose weight, causing a drop in leptin production, the brain will try and do what it can to bring that weight back up again. "The way it does this is by trying to reduce energy expenditure and increase food intake." The result is that when you compare two people who weigh the same, one of whom has just lost ten kilos, you will find that the newly lighter individual is hungrier and has a slower metabolism than the other person. Research at Columbia University in New York has shown that replacing the leptin reverses these metabolic effects, an idea that could be the focus of drug development to help people keep weight off.

With obesity affecting more than one-third of Americans and taking a toll on the nation's health care system, Perez-Tilve says the results of this study show "we need to change our way of thinking about how to use leptin as a potential target for therapy to treat obesity."

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