When mice eat a lot of fructose (like in sugary drinks), their gut bacteria make a chemical called acetate, which their liver uses to build new fat—without needing the usual pathway, and this acetate ends up being a major source of the fat’s building blocks.

When mice eat a lot of fructose (like in sugary drinks), their liver turns on a special enzyme called ACSS2 that helps turn gut bacteria’s waste product (acetate) into fat, making the liver store more fat.

When mice eat fructose (a sugar found in fruit and soda), their liver turns on genes that make fat—even if you block the usual ways the body processes sugar or remove gut bacteria. It’s like fructose itself has a secret signal that tells the liver to start making fat.

Eating a lot of sugar like high-fructose corn syrup makes your liver produce more fat than eating a lot of fatty foods does, and this happens in both people and mice.

When mice slowly eat a lot of fructose (a sugar found in fruit and soda), their livers start making more fat using two different biological tools—ACLY and ACSS2. To stop the liver from making extra fat, you have to block both tools at the same time.

When scientists removed the good bacteria from mice’s guts, the mice made way less fat from fructose (like sugar in soda), even though they still processed the sugar the same way — proving that the bacteria’s waste product, acetate, is the main building block for making fat in the liver without using the usual pathway.