Why?

From the linked study:

Editor’s summary
Excess dietary intake of fructose can lead to hepatic lipid accumulation and the development of steatotic liver disease. In zebrafish, Jackstadt et al. found that dietary glucose was converted to sorbitol in the intestine, which was subsequently converted to fructose in the liver in the absence of gut microbiota. Antibiotic treatment of zebrafish to deplete gut microbiota resulted in hepatic steatosis, an effect mimicked by high concentrations of exogenous sorbitol and attenuated by inhibiting sorbitol formation or by intestinal repopulation with sorbitol-degrading Aeromonas bacteria. These results indicate that sorbitol is derived from glucose in the zebrafish intestine, implicate gut microbiota in protecting against sorbitol-induced steatosis, and suggest that dietary sorbitol, which is used as a sugar substitute, may increase the risk of developing steatotic liver disease. —Wei Wong

Abstract
Metabolic dysfunction–associated steatotic liver disease (MASLD) is linked to a shift in the composition of the gut microbiome. Here, we found that depletion of the gut microbiome in adult zebrafish led to the development of steatotic liver disease in animals on standard diets. Using metabolomics and isotope tracing, we found that dietary glucose was converted to sorbitol by host intestinal cells. Although bacteria degraded sorbitol in control animals, sorbitol was transferred to the livers of fish when the gut microbiome had been depleted. Within the liver, sorbitol was converted into fructose 1-phosphate, which subsequently activated glucokinase and increased glycolytic flux, leading to increased hepatic glycogen and fat content. Inhibition of sorbitol production in microbiome-depleted animals was sufficient to prevent the development of steatotic liver, and colonizing the intestines of microbiome-depleted fish with sorbitol-degrading Aeromonas bacterial strains rescued the steatotic liver phenotype. Conversely, exogenous administration of high concentrations of sorbitol phenocopied gut microbiota depletion and induced hepatic steatosis. Together, these findings show that sorbitol-degrading bacteria in the gut protect against steatotic liver disease and suggest that excessive intake of dietary sorbitol may pose a risk for the development of MASLD.

They're implicating several types of natural sugars and saying that if you killed your gut microbiome with high concentration of sorbitol, then it might be bad for your liver. Ok??? Without any indication of the human-equivalent amounts involved, this is utterly useless. And this from a team who already went "HFCS feeds cancer!"? Seems like headline-chasers to me.

Also, since I read this earlier today:

The UK’s Scientific Advisory Committee on Nutrition in 2015 disputed the claims of fructose causing metabolic disorders, stating that “there is insufficient evidence to demonstrate that fructose intake, at levels consumed in the normal UK diet, leads to adverse health outcomes independent of any effects related to its presence as a component of total and free sugars.”[60]