Is This Metabolic Molecule from Pythons the Next Big Weight-Loss Drug?

If you visited a certain laboratory at Stanford University, you would find very slender mice. After ingesting a newly discovered compound identified by researchers in a study published this morning in Natural metabolismthe obese mice lost a lot of weight (relatively speaking, of course). Although our metabolisms are not a dead ringer for mouse metabolism, the compound’s effects in mice suggest that it could potentially become the next big weight loss drug for us humans.

Pathology researchers from the Stanford Lab, working with postdoctoral researchers from the University of South Florida and Colorado Boulder, studied how pythons undergo a series of changes related to digestion. Because pythons can eat massive meals and then don’t need to eat for a few months, they are metabolically adapted to extreme cycles of feast and famine. In blood samples from young Burmese pythons (Python bivittatus), researchers detected a metabolite molecule (pTOS) that increased more than a thousand-fold after a meal of about 25 percent of their body weight.

“We wondered whether this metabolite affects post-feeding physiological changes in the snake,” lead study author Jonathan Long explained in a press release. “But when we administered pTOS to laboratory mice at levels similar to those seen in pythons after eating, we saw no effects on energy expenditure, beta cell proliferation, or organ size.”

Read more: “The Secrets of Deadly Snake Bites”

However, mice given pTOS lost their appetite and 9% of their body weight during the 28-day monitoring period, while maintaining their water intake, energy level and movement. The effect mirrors that of GLP-1 drugs like Ozempic, but the researchers found the mechanism to be distinct. Semaglutide medications reduce the rate of emptying of the stomach to keep you feeling full longer. Python pTOS does not do this.

Instead, “pTOS is produced after a meal through tyrosine metabolism in the intestine and liver,” Long explained. “It then goes to a region of the brain called the hypothalamus, which is a well-known regulator of energy homeostasis.” Once in the hypothalamus, the pTOS python activates the neurons that regulate eating behaviors.

Looking at existing datasets of healthy human volunteers before and after meals, the researchers found that the majority (five out of six) had spikes in pTOS after eating. It’s typically only increased severalfold (again, compared to a thousandfold in pythons), an outlier experiencing a 25-fold increase. In fairness, though, since we eat only 1 to 2 percent of our body weight per meal, one might expect humans to have “a relatively narrow physiological and metabolic range” compared to pythons, Long said.

“Obviously we are not snakes,” he continued. “But perhaps by studying these animals we can identify molecules or metabolic pathways that also affect human metabolism.”

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