A new 2026 study published in Gut Microbes pulls together three research groups - Harvard Medical School, Massachusetts General Hospital, UC San Diego, Yale, and Duke - around a single gut enzyme: bile salt hydrolase, or BSH. The work matters because it connects three things that usually stay separate: the bacteria in your gut, the bile acids those bacteria reshape, and the barrier that keeps gut contents out of your bloodstream. When that barrier weakens in fatty liver disease, the study shows, the reshaped bile acids are part of the problem.
Bile salt hydrolase is an enzyme made by gut bacteria, not by human cells. Its job is to cut a molecule off bile acids - the process that turns conjugated bile acids into unconjugated ones. That single chemical change has downstream effects. The research team, led by A. Sloan Devlin and Raymond T. Chung, had already shown in lab models that unconjugated bile acids can damage the intestinal barrier, and that blocking BSH activity can restore it. The open question was whether the same chain of events happens in actual people with MASLD, and whether a small molecule could interfere with it.
What the study actually measured
The study ran in three connected layers. First, the team collected portal vein blood from 16 people with advanced cirrhosis who were undergoing a TIPS procedure, then measured bile acids with mass spectrometry. Portal blood is the blood that leaves the gut and heads straight to the liver - so it is the closest window onto what is crossing the intestinal wall. The average total bile acid there was about 116 micromoles per liter, far above the roughly 15 micromoles reported in people without liver disease, and unconjugated bile acids averaged about 28 micromoles. That is direct, human evidence that bile acids are crossing a leakier barrier.
Second, the team analyzed 111 stool samples from MASLD patients spanning fibrosis stages F0 through F4, measuring fecal bile acids, BSH enzyme activity under anaerobic conditions, and the 16S rRNA microbiome profile all at once. The point was to see whether BSH activity tracks with disease stage and which bacteria drive it. Third, they isolated bacterial strains from high-BSH stool samples and tested two small-molecule inhibitors, AAA-10 and GR-7, against both the patient-derived communities and single strains.
Why the gut barrier matters for the liver
The gut-liver connection works through a gate: the single layer of cells lining your intestine. When that layer is intact, bacteria and their byproducts stay in the gut. When it loosens - a state researchers call increased intestinal permeability - bacterial components and gut metabolites can slip through into the portal circulation and reach the liver, where they keep inflammation and fibrosis going. The BSH story slots into this: by converting bile acids, gut bacteria may be tipping the balance toward the forms that loosen the gate.
This is the same gut-liver axis this site has covered before, but the BSH paper adds a specific, druggable step. Because human cells have no equivalent enzyme, a BSH inhibitor would be selective for the microbiome - which is exactly why the team tested AAA-10 and GR-7. If a small molecule can reduce BSH activity, the reasoning goes, it could raise conjugated bile acids, tighten the barrier, and take pressure off the liver. That is a therapeutic idea, not a food one, and the distinction is worth keeping clear.
The food side of the same pathway
Even though the drug target is years from the clinic, the pathway points at real food levers. The bacteria that make BSH are shaped by what you feed them. Fiber is the main currency: legumes, whole grains, and vegetables feed the microbes that support a healthier gut environment, and the database rates all of those in the Recommended column. Fermented foods - plain yogurt, kefir, sauerkraut - contribute live cultures, and unsweetened plain yogurt rates Recommended in the database on its low saturated share and high protein.
The database gives the specific per-food numbers. Plain nonfat yogurt sits in the Recommended column at roughly 0.1 grams of saturated fat per 100 grams with meaningful protein; full-fat versions shift toward Moderation on saturated share. Rolled oats land in Recommended with fiber around 10 grams per 100 grams. Lentils and chickpeas are Recommended with both fiber and protein. These are the pattern foods that support the gut side of the axis, and they are the version of the science a reader can act on today.
How our editorial team read this
We treat mechanism papers with a specific discipline: they explain a pattern, they do not invent one. Our data editor walked through the three study layers and flagged what they establish and what they do not. The portal blood finding is genuine human evidence of bile acids crossing a compromised barrier - that is novel and specific. The BSH activity across F0-F4 is an association, not proof of causation. And the small-molecule inhibitors are preclinical tools, not treatments. None of that changes the food guidance, and it should not be read as a reason to start any supplement.
What we did not do is translate a bacterial enzyme target into a pill recommendation. The reader-facing version is simpler: the same fiber-and-fermented-foods pattern that supports the gut microbiome is already the Recommended column, and this study adds one more reason it holds. The therapeutic angle belongs in the clinic, not the pantry.
The practical takeaway
For someone managing MASLD, the BSH paper does not change the plate. It deepens the explanation. The gut barrier, the bile acids, and the bacteria are one connected system, and the dietary pattern that keeps that system healthy is the one the database has been rating all along: fiber at most meals, a low-fat fermented food in rotation, olive oil as the default fat, and the added-sugar veto enforced. The enzyme science is context; the pattern is the tool.