Many studies have recently shown that diet and its impact on gut microbiota are closelyrelated to obesity and metabolic diseases including nonalcoholic fatty liver disease. Gutmicrobiota may be an important intermediate link, causing gastrointestinal and metabolicdiseases under the influence of changes in diet and genetic predisposition. The aim of thisstudy was to assess the reversibility of liver phenotype in parallel with exploring theresilience of the mice gut microbiota by switching high-fat diet (HFD) to chow diet (CD). Micewere fed an HF for 8 weeks. A part of the mice was euthanized, whereas the rest were thenfed a CD. These mice were euthanized after 3 and 7 days of feeding with CD, respectively.Gut microbiota composition, serum parameters, and liver morphology were assessed. Eightweeks of HFD treatment induced marked liver steatosis in mice with a perturbedmicrobiome. Interestingly, only 7 days of CD was enough to recover the liver to a normalstatus, whereas the microbiome was accordingly reshaped to a close to initial pattern. Theabundance of some of the bacteria includingPrevotella,Parabacteroides,Lactobacillus, andAllobaculumwas reversible upon diet change from HFD to CD. This suggests thatmicrobiome modifications contribute to the metabolic effects of HFD feeding and thatrestoration of a normal microbiota may lead to improvement of the liver phenotype. Inconclusion, we found that steatosis and gut microbiota dysbiosis induced by 8 weeks ofhigh-fat diet can be reversed by 1 week of chow diet administration, and we identified gutbacteria associated with the metabolic phenotype