This is a microscope image of brown fat (e-BAT, or engineered Brown Adipose Tissue) created by adding a key control switch to skin cells of mice. Presence of green-stained objects (droplets of oil stored in the cell) confirms the skin cells have been converted to brown fat-producing cells. Blue objects are cell nuclei. Credit: Shingo Kajimura, Ph.D., Dana-Farber Cancer Institute

Researchers have developed a recipe for making brown fat, an energy-burning type of fat found mostly in infants and hibernating animals, and discovered that when injected into mice, it caused the cells to develop into brown fat tissue that burned excess energy. However, it's not yet clear whether the fat transplant can prevent these animals from gaining weight when on a high-calorie diet. The research was reported online today in the journal Nature.

White fat--the culprit behind beer bellies and dimpled thighs--stores excess energy from a person's diet. High levels of white fat, especially around the abdomen, can increase the risk for heart disease and diabetes. The primary role of brown fat, in contrast, is to generate heat, protecting newborns from the cold, for example. Scientists previously thought that only young animals had significant amounts of this tissue, but recent research using positron-emission tomography has shown that adults have a surprising amount of brown fat around the neck and chest. Because these cells burn calories, scientists have been searching for ways to turn up their activity as a potential treatment for obesity.

In the recent study, Bruce Spiegelman and colleagues at the Dana Farber Cancer Institute identified two proteins that work together to trigger development of brown fat. When researchers engineered genes for these two proteins into both mouse and human skin cells, the cells developed into brown fat.

According to a press release from Dana Farber:

The scientists then transplanted these synthetic brown fat precursors, known as eBAT (engineered [brown adipose tissue]), into adult mice to augment their innate stores of brown fat. Tests showed that the brown fat transplants were burning caloric energy at a high rate -- energy that otherwise would have been stored as fat in white adipose tissue.

"Since brown fat cells have very high capacity to dissipate excess energy and counteract obesity, eBAT has a very high potential for treating obesity," said Shingo Kajimura, PhD, lead author of the paper. "We are currently working on this."

... The experiments did not test whether the extra brown fat actually protected the mice from becoming obese.

For most, Thanksgiving is a time of overindulgence: from Grandma's specially roasted turkey and homemade gravy to Aunt Betty's prize-winning pumpkin pie, it's hard to say no to seconds. But researchers looking for a treatment for obesity have found a molecule that might well tell your brain that your stomach is full. So maybe if we listen more closely tomorrow, we won't suffer a postmeal food coma after all.

Researchers at the Yale School of Medicine and the University of Cincinnati conducted experiments with rats and mice and found that their small intestines release large quantities of a molecule called N-acylphospatidylethanolamine (NAPE) shortly after a fatty meal. This chemical apparently travels straight to the brain and puts a halt to further hunger signals. The researchers then synthesized NAPE and injected it into rats. After just five days of treatment, they showed a reduced appetite and significant weight loss. The findings are published today in the journal Cell.

Lead researcher Greg Shulman and his team are now monitoring NAPE levels in humans to see if they rise the same way after a big meal. Ultimately, their studies could help researchers design better appetite suppressants or obesity-fighting drugs.

From the press release:

The team used Shulman's lipid analysis system to investigate what happens to fat that enters the blood after ingesting a high-fat meal. The scientists reasoned that the fat derivatives that enter the bloodstream might themselves serve as messengers to signal the brain that the body has been fed. They used this approach to compare the lipids present in blood plasma from rats that had fasted or eaten, and they zeroed in on NAPE.

They found only low levels of NAPE in the blood of rats that had fasted for 12 hours. The level of NAPE shot up 40 to 50 percent in animals that had dined on high-fat chow. Furthermore, NAPE didn't increase in rodents that ate only protein or carbohydrate, suggesting that NAPE levels reflect the amount of fat eaten in a meal.

The researchers found that when they injected synthetic NAPE into the abdominal cavity or blood, the rodents' appetites diminished substantially. The more NAPE they received, the less food they ate. "It's really quite effective," Shulman says. "At the highest doses, it keeps the animals from eating for up to 12 hours." At a low dose--comparable to the spike in NAPE that occurs naturally after a meal--the rodents still ate 25 percent less than controls. They even acted full, going into "siesta mode" as if they had just eaten, Shulman says, noting that additional tests confirmed that the animals were only lethargic, not ill or incapacitated.

When the researchers delivered tiny amounts of NAPE directly into the brain, it had the same effect as a larger dose delivered to the blood. This suggests that the compound communicates directly with the brain, Shulman says.

There has been much debate about the best policies for reducing carbon emissions. The most common refrain heard from economists is simply that incentives matter: if gas prices increase, people will consume less gasoline (by driving less), and alternative fuels will become more feasible substitutes (by having a more competitive price).

While an increase in the gas tax remains a point of contention, not only among economists, but also among politicians and policy wonks, now supporters of a gas tax have another reason to offer to strengthen their argument: an increase in the price of gas will most likely lead to a less obese population.

In a recent research paper, Charles Courtemanche, an economist at the University of Washington, St. Louis, provides the empirical support. He writes,

"A causal relationship between gasoline prices and obesity is possible through mechanisms of increased exercise and decreased eating in restaurants. I use a fixed effects model to explore whether this theory has empirical support, finding that an additional $1 in real gasoline prices would reduce obesity in the U.S. by 15% after five years, and that 13% of the rise in obesity between 1979 and 2004 can be attributed to falling real gas prices during this period. I also provide evidence that the effect occurs both by increasing exercise and by lowering the frequency with which people eat at restaurants."