An Australian research team has discovered a new method to treat obesity by directly blocking a fat cell receptor and accelerating energy consumption.
Research has already led to the development of an experimental drug that directly targets this receptor, and it has been effective in preventing obesity in mouse tests.
Fat cells are targeted
Il neuropeptide Y (NPY) is a peptide produced by the central nervous system known to play a role in various physiological processes.
High levels of NPY are linked to increased appetite and weight, while low levels increase energy expenditure, helping the body burn fat instead of storing it.
NPY is a regulator of metabolism in fat cells. It plays a critical role during low-energy states, as it helps to store fat as a survival mechanism.
Herbert Herzog, senior co-author of the new study.
Today, however, these beneficial effects can affect fat cells and produce weight gain even when dieting, leading to obesity and metabolic diseases.
Block a receptor and lose all unnecessary weight
One of the key cellular receptors that NPY uses to exert its effects is called Y1. The new study set out to explore whether blocking the Y1 receptor in peripheral tissues increased fat metabolism, preventing weight gain.
The researchers tested an experimental drug called BIBO3304 on mice.
The drug was designed to block Y1 signaling in fat cells.
Yan Churn Shi, senior co-author of the new study, says that after about seven weeks on a high-fat diet, the mice treated with BIBO3304 had gained 40% less weight compared to a control group with the same diet.
This significant reduction in body weight gain was caused by increased body heat generation and reduction in fat mass
Yan Churn Shi
Does it also work on human fat cells? It seems so.
“When we applied BIBO3304 to human fat cells isolated from obese individuals,” the researchers say, “the fat cells activated the same genes involved that produce body heat in mice. This suggests that targeting the Y1 receptor pathway could increase fat metabolism and reduce weight gain in humans as well.”
The most promising aspect of the new research is that the mechanism appears truly “surgical”. Y1 receptor signaling appears to be limited to fat cells.
Previous attempts to inhibit NPY mechanisms have led to extensive systemic side effects, making it unfeasible as a treatment anti-obesity, but this target, the Y1 receptor, may be the key to making everything work.
Not just obesity: side benefits
If BIBO3304 is a scourge for fat cells, for the rest of the human body it could be a panacea. Not only did the researchers find that the drug does not cross the blood-brain barrier, meaning it will not disrupt other NPY processes in the brain, but there may be secondary benefits to blocking Y1 signaling, including improvements in insulin resistance and function cardiovascular.
Of course there is still work to be done before the anti-obesity drug can be tested in vivo on humans. The potential for preventing obesity, however, is gigantic.
“Most current drugs used to treat obesity target the brain to suppress appetite and can have serious side effects that limit their use,” Shi says. “Our study reveals an alternative approach that directly targets fat cells, a safer way to prevent and treat obesity.”