The appeal of the Atkins diet is undeniable. Losing weight while being able to eat a high fat, low-carbohydrate diet was a revelation for butter and meat lovers when it peaked in popularity during the 1990s.

This, and other similar "ketogenic" diets, is founded on the understanding of ketosis - when the body's metabolism switches from carbohydrates to ketone bodies, which are produced from fatty acids that come out of storage in fat tissue and are transferred to the liver. This metabolic state is the same as the one produced when mammals go through periods of fasting, or starvation.

Now, two new studies published in the June issue of Cell Metabolism, have identified the "starvation hormone" that allows this process to occur. Understanding this hormone may be the beginning of breakthroughs for drug development to regulate metabolism and even glucose levels in the bloodstream.

One study, led by Eleftheria Maratos-Flier, MD, an investigator in the department of endocrinology, diabetes and metabolism at Beth Israel Deaconess Medical Center and associate professor of medicine at Harvard Medical School, found that mice fed a low carbohydrate, high fat (but no trans fat) diet still maintained normal levels of lipids in the circulatory system.

"The mice on this diet only had very modest weight loss, but they had normal levels of circulating lipids," Maratos-Flier said. " It seems if you're eating a lot of fat, but your insulin levels are low, there's a very effective system for burning the fat in the liver so it doesn’t end up in circulation."

The researchers identified all of the mice had an increased level of FGF21, a hormone produced in the liver. The higher rates of this hormone protected the mice from obesity, which raises the question of what could be accomplished if this hormone could be raised while maintaining a diet with carbohydrates.

The release of this hormone allows the liver to burn the fat that is being eaten, instead of it finding its way to the circulatory system where it can raise cholesterol.

Dr. Steven Kliewer, professor of molecular biology and pharmacology at UT Southwestern, led a the other study that found mice given this hormone stayed very thin even though they were on a regular diet.

"The remarkable thing is that mice that have high levels of this FGF21 looks like they're fasted or starved when they're fat," Kliewer said. "So this one hormone is enough to change the metabolic profile of the animal."

Most importantly, the release of this hormone demonstrates how the body can alter its metabolic process. When FGF21 was inhibited in mice by the Harvard team, they developed massive accumulation of fat in the liver and a spike in lipids in the bloodstream.

Even more exciting, when UT Southwestern researchers increased FGF21 levels in the mice, they found the mice actually lost weight. The regulation of this hormone could be revolutionary for people genetically-predisposed to obesity.

The breakthrough is that this hormone does even more than expected. Kliewer pointed to research by the pharmaceutical company Eli Lilly that showed this hormone not only lowers fat and cholesterol in the blood, but also decreases glucose in the blood in both monkeys and rodents.

"It does so many different things, it's affecting fat tissue, liver and it's probably affecting the brain," Kliewer found. "We were surprised, no one predicted there'd be a hormone coming out of the liver that would coordinate all these processes."

Once researchers learn more about how this hormone operates in humans, the applications could range from type 2 diabetes to fatty liver disease and obesity. Even with all there is left to know, Kliewer still felt "this molecule is really quite promising."