Obesity epidemic
Neuroscientists identify protein that inhibits appetite suppressor in the brain.Reuters

A treatment for obesity is edging closer, scientists said after they identified a protein in the brain involved in regulating food intake and body weight.

The Overseas Development Institute said that obesity in the developed world has quadrupled in the last 30 years to one billion.

In the UK, 64% of adults are classed as being overweight or obese.

However, a treatment to help stop the obesity epidemic may soon be at hand after the protein - alpha2/delta-1, which has never been linked to obesity before – was identified as being involved in food intake by neuroscientists at Tufts University School of Medicine in Boston.

The team believes this protein may also explain why some medications that interfere with this protein can cause weight gain.

Led by Maribel Rios, the team found that alpha2/delta-1 facilitates the function of another protein called brain-derived neurotrophic factor (BDNF), which plays a critical role in appetite suppression. When BDNF is inhibited, researchers found a central mechanism leads to overeating.

They found low levels of BDNF were associated with decreased function of alpha2/delta-1.

When the team inhibited alpha2/delta-1 in mice, they ate significantly more food and gained weight. When corrected, the mice went back to eating normally.

"The mice ate 39 percent more food, and as a consequence gained substantially more weight than control mice over a seven-day period."

"We know that low levels of the BDNF protein in the brain lead to overeating and dramatic obesity in mice," Rios said. "Deficiencies in BDNF have also been linked to obesity in humans. Now, we have discovered that the alpha2/delta-1 protein is necessary for normal BDNF function, giving us a potential new target for novel obesity treatments."

Joshua Cordeira, first author of the study, said: "We blocked activity of the alpha2/delta-1 protein in mice using gabapentin. These mice ate 39 percent more food, and as a consequence gained substantially more weight than control mice over a seven-day period."

Rios continued: "When we re-introduced alpha2/delta-1 in obese mice lacking BDNF in the brain, we saw a 15-20 percent reduction in food intake and a significant reduction in weight gain. Importantly, metabolic disturbances associated with obesity, including hyperglycemia and deficient glucose metabolism, were greatly reduced by restoring the function of alpha2/delta-1."

The researchers are now looking to better understand alpha2/delta-1's role in appetite so they can develop treatments that stop weight gain among people taking drugs such as gabapentin and pregabalin, which often lead to weight gain as a side effect.

"We now know that alpha2/delta-1 plays a critical role in healthy BDNF function. The finding improves our understanding of the intricate neuroscience involved in appetite control. The next phase of our research will be to unravel the mechanisms mediating the satiety effects of alpha2/delta-1 in the hypothalamus," Rios said.