Abstract
Dietary habits and gut microbiota play an essential role in non-alcoholic fatty liver disease (NAFLD) and related factors such as insulin resistance and de novo lipogenesis. In this study, we investigated the protective effects of Bacteroides uniformis CBA7346, isolated from the gut of healthy Koreans, on mice with high-fat diet (HFD)-induced NAFLD. Administration of B. uniformis CBA7346 reduced body and liver weight gain, serum alanine aminotransferase and aspartate aminotransferase levels, liver steatosis, and liver triglyceride levels in mice on an HFD; the strain also decreased homeostatic model assessment for insulin resistance values, as well as serum cholesterol, triglyceride, lipopolysaccharide, leptin, and adiponectin levels in mice on an HFD. Moreover, B. uniformis CBA7346 controlled fatty liver disease by attenuating steatosis and inflammation and regulating de novo lipogenesis-related proteins in mice on an HFD. Taken together, these findings suggest that B. uniformis CBA7346 ameliorates HFD-induced NAFLD by reducing insulin resistance and regulating de novo lipogenesis in obese mice.
Highlights
IntroductionThe global prevalence of Non-alcoholic fatty liver disease (NAFLD) is increasing at a rate comparable to that of type 2 diabetes mellitus and obesity, and is estimated to be present in 25% of adults [2]
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, characterized by irregular lipid accumulation in hepatocytes even without alcohol abuse [1].The global prevalence of NAFLD is increasing at a rate comparable to that of type 2 diabetes mellitus and obesity, and is estimated to be present in 25% of adults [2]
The p-AMPKα/AMPKα ratio was significantly higher in the HU group than in the HC group (p < 0.05). These results suggest that B. uniformis CBA7346 alters high-fat diet (HFD)-induced changes in hepatic lipid metabolism
Summary
The global prevalence of NAFLD is increasing at a rate comparable to that of type 2 diabetes mellitus and obesity, and is estimated to be present in 25% of adults [2]. As NAFLD progresses, serious liver diseases including hepatic inflammation, hepatic fibrosis, cirrhosis, liver failure, and liver cancer develop [3]. A variety of factors including dietary habits such as a high-fat diet (HFD), and genetic and environmental factors, can lead to obesity accompanied by insulin resistance and adipocyte proliferation [4]. Insulin resistance plays a key role in the pathogenesis of steatosis, and increases hepatic de novo lipogenesis [5]. Controlling insulin resistance and inhibiting the de novo lipogenesis pathway could reduce hepatic steatosis in obese individuals
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