Eat Whatever You Want. the “Exercise Pill” Is Almost Here.

There is no denying that obesity has reached a pandemic stage. The good news is that, like any medical condition, obesity might soon be cured by simply taking a pill.

Two recent studies give us hope. The first one comes from Canada. Michigan Medicine researchers at the University of Michigan discovered that a protein called Sestrin can mimic physical exercises’ effects in flies and mice. The scientists put a bunch of flies to work out, climbing up and out of a test tube. They compared the running and flying ability of normal flies with that of flies bred to lack the ability to make Sestrin.

“Flies can usually run around four to six hours at this point and the normal flies’ abilities improved over that period,” says prof. Jun Hee Lee at the Department of Molecular & Integrative Physiology. “The flies without Sestrin did not improve with exercise.”

But the beneficial effects of Sestrin include more than just improved endurance. Mice without Sestrin lacked the improved aerobic capacity, improved respiration, and fat burning typically associated with exercise.

Does this mean that Sestrin supplements are on their way to the market? Not yet. Scientists still don’t know how exercise produces Sestrin in the body. But future studies are on the horizon, searching for small molecule modulators of Sestrin. This could lead to a treatment for people who cannot exercise.

In a second study, researchers at Dartmouth’s Norris Cotton Cancer Center observed that blocking a cellular receptor reversed obesity, with no ill side effects, in mice. In case you were wondering why a Cancer Center is concerned with obesity, you should remember that obesity is a major risk factor associated with several cancers, including breast, colon, and pancreatic.

The scientists carried out experiments showing that when a drug named NF, known to block a specific cellular receptor, was added to a high-fat diet, mice did not become any fatter than mice on a low-fat control diet. On the other hand, mice on the high-fat diet that weren’t treated with NF became very obese within the same time span. No adverse effects were observed from the drug.

But then the team was curious to find out if blocking the cellular receptor in question with NF could not only prevent obesity but reverse it. So they allowed the mice to become obese on a high-fat diet, and then half the mice were switched to the high-fat diet containing the drug, while the other half were kept as a control group. Over the next few weeks, the mice switched to the high-fat diet containing the drug dropped to the same body weight as those mice on the low-fat diet. The remaining mice on the high-fat diet remained obese. Again, no ill effects were observed.

Furthermore, the researchers discovered that in liver cells and in fat cells, the investigated cellular receptor, when blocked by NF, fails to induce several key genes required for fat storage and synthesis. Now they are trying to respond to another two important questions: what compounds in our diet activate this cellular receptor to cause obesity, and what role has the gut microbiome in this activation.

Most importantly, a clinical trial has begun, in order to determine whether the AHR may serve as a therapeutic target to reduce obesity in humans.