Scientists are still discovering how weight loss “wonder drugs” like Ozempic and Zepbound reshape the body.
Researchers at the Salk Institute have found that long-term use of these drugs reprograms cells and produce long-lasting and potentially beneficial changes that extend far beyond weight loss.
Sam Van de Velde, PhD, , first author of a paper on the subject, featured in the Proceedings of the National Academy of Sciences, has spent five years searching for the “next piece of the puzzle.”
“They seem to be doing a lot of things at once. Scientists don’t really like those ‘wonder, miracle’ terms. We prefer not wondering about anything — just understanding the whole thing,” said Van de Velde.
Sam Van de Velde photographed in his Salk Institute laboratory. (Photo by Thomas Murphy / Times of San Diego)More than 30 million Americans use these drugs, according to KFF. Gallup reports their use doubled from 2024 to 2025, and is still rising.
Originally developed to treat type 2 diabetes, these drugs mimic chemical signals created by the gut after eating food, known as GLP-1. Today, they are better known for their weight-loss side effect, which limits appetite, resulting in changes to eating habits.
Stability is the key difference between the natural and injected chemicals, meaning the drug lasts in the body longer. Scientists first discovered the stable version in the saliva of the Gila monster, one of only two known venomous lizard species in the world.
When this chemical reaches the pancreas, it is picked up by small clusters of beta cells. These release insulin, which helps cells absorb sugar to regulate blood sugar; think of them as sugar sensors.
“Type 2 diabetes occurs when your blood sugar and level of fat particles in your blood goes up; these are toxic to the beta cells, they decline in health. Stable GLP-1 drugs increase the health of the beta cells and increase their insulin production capacity,” said Van de Velde.
The drug must attach to the beta cells for this communication to happen. This attachment causes a process called phosphorylation — a small chemical modification that adds a phosphate group to a protein, affecting how it works.
The team focused on a specific protein complex, Med14, which mediates gene activation. In this case, it is part of the body’s insulin production in the pancreas. It is known as a “conserved protein.”
“There’s Med14 in chickens, yeast, all kinds of fungi, and, of course, people. They cannot survive without it; the body won’t develop — that’s how essential it is,” said Van de Velde.
“We find that on this protein, a tiny chemical modification occurs when the cells are treated with the GLP-1 drug, which allows for hundreds of genes to simultaneously be turned on. We call this the genomic response, that’s what programs the beta cells to perform better in challenging conditions,” said Van de Velde.
Sam Van de Velde using a laboratory microscope that takes basic images of cells. (Photo by Thomas Murphy / Times of San Diego)Just one injection isn’t enough; it requires long-term use. The changed beta cells produce more insulin and become more resilient to toxic high blood sugar levels.
To prove their discovery, which was part of the study published in PNAS, the Salk team started work on a comparison to prove Med14’s essential role. They made a minor mutation to the pancreatic beta cells of mice, preventing the chemical modification that usually happens in response to the drug. The number of cells fell, weakening their insulin production.
“We basically turned the switch so it is always off; it is not responsive to GLP-1 drugs anymore,” said Van de Velde.
While this was proven in mice, the results likely apply for humans too.
Small (left) and large (right) condensates of Med14 inside nuclei of pancreatic beta cells. (Image courtesy of Salk Institute)This discovery has deepened the understanding of GLP-1’s effects on the human body, there are more questions to be answered.
“There is evidence that this effect disappears when you stop taking the drugs, but there’s also evidence that it doesn’t disappear entirely. People lose weight on the drug, go off, and gain weight again, but they don’t go back to their initial levels. There’s reason to believe the cells enter a more permanent state after long-term use, which is beneficial for patients,” said Van de Velde.
The understanding of these drugs has not kept pace with their widespread use. As they are prescribed more and more, researchers discover new potential benefits: blocking inflammation, reducing fatty liver disease and potentially lowering the chance of neurodegenerative disease.
Side effects include nausea and other stomach issues, usually fixed by changing dosages or cutting out fatty foods from the diet. Patients must consult with a doctor or healthcare provider before starting and while taking these medications.
Fully grasping how these drugs work could lead to new therapies, so Van de Velde’s work is vital.
“Understanding the mechanism by which they work will show us how these drugs do all these things they can do, which could lead to new therapies,” said Van de Velde. “For us, since we’re investigating Med14, we would ask if this works throughout the body, like the part of the brain that controls appetite. That area has receptors for GLP-1 and is known to block your food urges or desires — it can also block addictive behaviors like alcoholism.”
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