Chowing down on a high-fat diet may not only grow your waistline. It may also plump stem cell populations in your gut—cells that are prone to producing tumors.

After about a year of feeding mice a diet of 60 percent fat, researchers found that the rodents had an unusually hefty population of cancer-susceptible intestinal stem cells and cells that act like stem cells. Those cells were supercharged by a protein called PPAR-δ, which can be switched on by the presence of fatty acids in the gut, the researchers reported.

The findings, published in Nature, may explain why epidemiological data in humans has repeatedly linked obesity to boosted risks of cancer, particularly colon cancer. It may also offer researchers a new target for knocking back the risks of cancer in the obese.

In the gut, there is usually a tiny pocket of stem cells that works to replenish the cells that line the intestine. These cells hang around for a lifetime, giving them extra opportunities to acquire mutations that could spur tumors.

In the fat-fed mice, which grew chubby, this tiny stem cell population unexpectedly flourished. And, progenitor cells—specialized progeny of stem cells—started acting more like their parents, too. They lived longer, upping their opportunities to acquire mutations and tumor-spawning potential.

The researchers found that PPAR-δ was behind that boom in stem and progenitor cells. In petri-dish experiments, the researchers found that fatty acids from the high-fat diet increased the amounts of PPAR-δ cells were making.

That makes sense because the protein is known to switch on metabolic machinery that helps burn fat over carbohydrates. But the protein also seems to spark specific genetic changes that ignite the two cell populations, the researchers suggest.

In their fat mice, the researchers noted higher rates of spontaneous tumors than in control mice.

Still, the researchers will need to do more work to know if PPAR-δ and the stem cells explain the link between cancer and obesity in humans.

Nature, 2015. DOI: 10.1038/nature.2016.19484 (About DOIs).