Abstract
Many studies have recently shown that diet and its impact on gut microbiota are closely related to obesity and metabolic diseases including nonalcoholic fatty liver disease. Gut microbiota may be an important intermediate link, causing gastrointestinal and metabolic diseases under the influence of changes in diet and genetic predisposition. The aim of this study was to assess the reversibility of liver phenotype in parallel with exploring the resilience of the mice gut microbiota by switching high-fat diet (HFD) to chow diet (CD). Mice were fed an HF for 8 weeks. A part of the mice was euthanized, whereas the rest were then fed 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. Eight weeks of HFD treatment induced marked liver steatosis in mice with a perturbed microbiome. Interestingly, only 7 days of CD was enough to recover the liver to a normal status, whereas the microbiome was accordingly reshaped to a close to initial pattern. The abundance of some of the bacteria including Prevotella, Parabacteroides, Lactobacillus, and Allobaculum was reversible upon diet change from HFD to CD. This suggests that microbiome modifications contribute to the metabolic effects of HFD feeding and that restoration of a normal microbiota may lead to improvement of the liver phenotype. In conclusion, we found that steatosis and gut microbiota dysbiosis induced by 8 weeks of high-fat diet can be reversed by 1 week of chow diet administration, and we identified gut bacteria associated with the metabolic phenotype.
Highlights
Henao-Mejia et al [7] provided evidence that modulation of the intestinal microbiota through multiple inflammasome components is a critical determinant of nonalcoholic fatty liver disease (NAFLD) and NASH progression, whereas it has been demonstrated the gut microbiota protects against steatohepatitis in the methioninecholine–deficient model [8]
7 days of chow diet (CD) led to a new cluster (7d-CD-Tf) closer but slightly different from the original one. These results indicate that high-fat diet (HFD) strongly affects gut microbiota composition, which is partially restored by 1 week of CD
In the experimental setup used in this study, mice were fed HFD for 8 weeks followed by a change to CD to first describe how HFD affects body weight gain, liver phenotype, and gut microbiota composition in mice and to evaluate the reversibility of these HFD-induced effects
Summary
involvement of the microbiota in NAFLD development [4]. In an early study, Drenick et al [5] observed hepatic steatosis development in patients undergoing gastric bypass surgery that coincided with bacterial overgrowth. Small intestinal bacterial overgrowth has been shown to be more prevalent in patients with NASH than in healthy controls [6]. Henao-Mejia et al [7] provided evidence that modulation of the intestinal microbiota through multiple inflammasome components is a critical determinant of NAFLD and NASH progression, whereas it has been demonstrated the gut microbiota protects against steatohepatitis in the methioninecholine–deficient model [8]. We have further revealed that the propensity to develop NAFLD directly depends on gut microbiota composition, independently of obesity [9]. These findings suggest that high-fat diet (HFD) alone is not sufficient to cause obesity or NAFLD development and that the gut microbiota contributes to these diet-induced metabolic disorders
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