Abstract
High fructose diet causes metabolic syndrome and induces host gut microbial dysbiosis and related obesity and nonalcoholic fatty liver disease (NAFLD). Several antibiotic treatments could prevent fatty liver. However, there are studies that have demonstrated that a high-fructose diet could influence the gut microbial dysbiosis and induce fatty liver. The purpose of this study was performed to partially modify the gut bacterial composition with a single cefotaxime treatment, which might affect the fructose-induced NAFLD severity. The C57BL/6JNarl male mice were divided into four groups including vehicle/chow diet (VE-CD), vehicle/high-fructose diet (VE-FD), antibiotic (cefotaxime (CF))/CD, and CF/FD. The results showed that body weight gain, moderate hepatic steatosis severity, epididymal white adipose tissue hypertrophy, and insulin resistance occurrence with NAFLD-related symptoms were observed only in the CF-FD group. The raised protein expression of hepatic lipogenesis was observed in the CF-FD group, but lipolysis protein expression was no difference. The diversity and composition of microbiota were significantly reduced in the CF-FD group. The Erysipelatoclostridium, Enterobacteriaceae, Lachnospiraceae, and Escherichia Shigella were in increased abundance in the feces of CF-FD group compared with VE-FD group. The novel model reveals that particular antibiotics such as cefotaxime co-treatment with high-fructose diet may affect the gut microbiota accelerating the NAFLD and obesity.
Highlights
IntroductionFructose is a type of ketonic monosaccharide present in various plants and fruits; it is the sweetest structure among all naturally occurring carbohydrates
The masses of epididymal white adipose tissue, inguinal subcutaneous WAT, perinephric WAT, and total measurement WAT were significantly larger in the CF-fructose diet (FD) group than in the vehicle/high-fructose diet (VE-FD) group (Table 1)
This study demonstrates that cefotaxime could induce composition changes in the gut microbiota, which could further affect the physiological and metabolic profiles of liver lipogenesis under high-fructose consumption
Summary
Fructose is a type of ketonic monosaccharide present in various plants and fruits; it is the sweetest structure among all naturally occurring carbohydrates. High fructose consumption is considered an indicator of Western diets; it induces metabolic syndrome in gut microbial dysbiosis. During 1977–1978, the fructose consumption increased from 8% to 10.2% of the total calorie intake The consumption of fructose was the highest, increasing up to 12.1% of the total calorie intake (72.8 g/d). Over 10% of the Americans’ daily calories originate from fructose [1]. The high fructose consumption is associated with diseases including nonalcoholic fatty liver disease (NAFLD), type 2 diabetes mellitus (T2DM), and metabolic syndrome [2,3,4]
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