Whenever you feel really happy (like too happy) or even just healthy and content, your brain is releasing the neurotransmitter serotonin. But while this form of serotonin is the most popular, it only makes up five percent of the body’s total supply. The other 95 percent, a new study finds, is busy regulating how well your body burns calories through brown fat.
Stored around your collarbone are deposits of brown adipose tissue (fat) that help burn energy. Brown fat is scarcer in obese people, and for years researchers have wondered about the mechanism behind the reduction. Recently, a team from McMaster University has found the presence of so-called “peripheral serotonin” makes brown fat less active due to enzyme blockage.
“Too much of this serotonin acts like the parking brake on your brown fat,” said Gregory Steinberg, a professor of medicine and the paper’s co-author, in a statement. “You can step on the gas of the brown fat, but it doesn’t go anywhere.”
Brown fat was once believed to be a vestige of evolution — similar to the appendix — that helped keep warm other mammals that do not shiver. But several years of research have begun confirming brown fat’s advantages, principally a role in speeding up the body’s metabolism. As we age, however, the stores of beneficial brown fat, which burn the “bad” white fat that accumulates on our bellies and thighs, begin to diminish. And depending on our diets, they could stop working entirely.
As of late, these concerns have multiplied for researchers involved with obesity. In the U.S. alone, more than one-third of adults, or 79 million people, are obese. The annual cost for treating the conditions associated with obesity, including heart disease, stroke, type 2 diabetes, and some types of cancer, totals $147 billion in 2008 dollars, the latest year for which data are available. Individually, medical costs for the obese are $1,429 higher than for those of a normal weight.
Given these concerns, Steinberg and his colleagues wanted to understand how exactly brown fat’s energy burning comes to a halt. Previous work in their lab had shown the enzyme tryptophan hydroxylase, or Tph1, was overrepresented in lighter mice. Using Tph1 in their follow-up studies, they fed a second group of mice a high-fat diet that was designed to mimic a traditional Western diet. Those with the enzyme mutation produced less serotonin than the normal mice, in turn keeping them healthier.
“What we discovered is that if we remove this enzyme either genetically or if we inhibit its activity using a chemical, a drug, the mice have low levels of serotonin and they didn’t develop diabetes, obesity, or fatty liver disease,” Steinberg said.
This finding holds great promise for future weight loss drugs, the team argued. Most of the current options rely on suppressing people’s appetites to achieve a desired amount of weight loss. They also produce severe side effects, including heart complications and risks for depression. Inhibiting the enzyme that triggers energy storage tackles the problem from the other direction, helping to increase the amount of energy people burn normally.
“Moving forward, we think it’s a much safer method to work with increasing energy expenditure instead of decreasing the appetite, which involves more risks,” Steinberg said. He and his team are currently at work on a pharmacological approach that could stand in as a substitute for traditional weight loss pills.
Source: Crane J, Palanivel R, Mottillo E, et al. Inhibiting peripheral serotonin synthesis reduces obesity and metabolic dysfunction by promoting brown adipose tissue thermogenesis. Nature Medicine. 2014.
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