We used cross‐sectional and longitudinal studies to comprehensively compare hepatic steatosis measurements obtained with magnetic resonance imaging–proton density fat fraction (MRI‐PDFF) and controlled attenuated parameter (CAP) in hepatic steatosis in adults with nonalcoholic fatty liver disease (NAFLD). A total of 185 participants with NAFLD and 12 non‐NAFLD controls were recruited. CAP and MRI‐PDFF data were collected at baseline from all participants and from 95 patients included in the longitudinal study after 24 weeks of drug or placebo intervention. Pearson correlation, linear regression, and piecewise linear regression analyses were used to evaluate the relationship between the two modalities. Linear analysis suggested a positive correlation between CAP and MRI‐PDFF (r = 0.577, p < 0.0001); however, piecewise linear regression showed no correlation when CAP was ≥331 dB/m (p = 0.535). In the longitudinal study, both the absolute and relative change measurements were correlated between the two modalities; however, the correlation was stronger for the relative change (relative r = 0.598, absolute r = 0.492; p < 0.0001). Piecewise linear regression analysis revealed no correlation when CAP was reduced by more than 53 dB/m (p = 0.193). Conclusions: We found a correlation between CAP and MRI‐PDFF measurements for grading hepatic steatosis when CAP was <331 dB/m. While the measured absolute change and relative change were correlated, it was stronger for the relative change. These findings have implications for the clinical utility of CAP or MRI‐PDFF in the clinical diagnosis and assessment of NAFLD.

Non-alcoholic fatty liver disease (NAFLD) remains a common disease with a significant health and economic burden worldwide. The gut microbiota (GM) and bile acids (BAs), which play important roles in the gut-liver axis, have been confirmed to jointly participate in the development of NAFLD. GM not only regulate bile acids’ synthesis, transport, and reabsorption by regulating other metabolites (such as trimetlyl amine oxide, butyrate), but also regulate dehydrogenation, dehydroxylation and desulfurization of bile acids. Meanwhile, disordered bile acids influence the gut microbiota mainly through promoting the bacterial death and lowering the microbial diversity. Although weight loss and lifestyle changes are effective in the treatment of NAFLD, the acceptability and compliance of patients are poor. Recently, increasing natural plants and their active ingredients have been proved to alleviate NAFLD by modulating the joint action of gut microbiota and bile acids, and considered to be promising potential candidates. In this review, we discuss the efficacy of natural plants in treating NAFLD in the context of their regulation of the complex interplay between the gut microbiota and bile acids, the crosstalk of which has been shown to significantly promote the progression of NAFLD. Herein, we summarize the prior work on this topic and further suggest future research directions in the field.

Non-alcoholic fatty liver disease (NAFLD) is a liver disorder characterized by abnormal accumulation of hepatic fat and inflammatory response with complex pathogenesis. Over activation of the pyrin domain-containing protein 3 (NLRP3) inflammasome triggers the secretion of interleukin (IL)-1β and IL-18, induces pyroptosis, and promotes the release of a large number of pro-inflammatory proteins. All of which contribute to the development of NAFLD. There is a great deal of evidence indicating that plant-derived active ingredients are effective and safe for NAFLD management. This review aims to summarize the research progress of 31 active plant-derived components (terpenoids, flavonoids, alkaloids, and phenols) that alleviate lipid deposition, inflammation, and pyroptosis by acting on the NLRP3 inflammasome studied in both in vitro and in vivo NAFLD models. These studies confirmed that the NLRP3 inflammasome and its related genes play a key role in NAFLD amelioration, providing a starting point for further study on the correlation of plant-derived compounds treatment with the NLRP3 inflammasome and NAFLD.