Abstract
In this study, the effects of a polysaccharide derived from Laminaria japonica (LJP) on obesity were investigated in mice fed a high-fat diet (HFD). LJP significantly attenuated obesity-related features, lowering serum triglycerides, glucose, total cholesterol and low-density lipoprotein cholesterol levels. HFD-induced liver steatosis and hepatocellular ballooning were significantly attenuated by LJP. Additionally, LJP was found to significantly modulate hepatic gene expressions of AMPK and HMGCR, which are key regulators of lipid and cholesterol metabolism. We further found that LJP ameliorated HFD-induced gut microbiota (GM) dysbiosis by significantly reducing the obesity-related Firmicutes to Bacteroidetes ratio, meanwhile promoting the growth of Verrucomicrobia at the phylum level. At the genus level, propionate-producing bacteria Bacteroides and Akkermansia were elevated by LJP, which might explain the result that LJP elevated fecal propionate concentration. Taken together, these findings suggest that dietary intake of LJP modulates hepatic energy homeostasis to alleviate obesity-related nonalcoholic fatty liver disease associated with GM regulation.
Highlights
Worldwide obesity has nearly tripled since 1975 [1]
To assess the impact of Laminaria japonica (LJP) on hepatic pathological changes caused by high-fat diet (HFD), liver sections were stained with haematoxylin and eosin (H&E) and the results showed that macrovesicular steatosis and ballooning degeneration were severe in the liver of HFDfed mice but were reduced dose-dependently in the liver of mice treated with LJP
To assess the impact of LJP on hepatic pathological changes caused by HFD, liver sections were stained with haematoxylin and eosin (H&E) and the results showed that macrovesicular steatosis and ballooning degeneration were severe in the liver of HFD-fed mice but were reduced dose-dependently in the liver of mice treated with LJP
Summary
The prevalence of obesity has raised a global concern over the challenge to prevent chronic diseases, such as heart disease, diabetes, high blood pressure and certain cancers [2]. Nonalcoholic fatty liver disease (NAFLD) is rapidly becoming the most common cause of chronic liver disease due to an increase in the prevalence of obesity [3]. Recent studies have implicated the gut microbiota (GM) as a critical player, since it modulates nutrient uptake, energy homeostasis and chronic metabolic disorders [4]. Considerable evidence that GM dysbiosis contributes to the pathogenesis of NAFLD has been provided by animal and human studies. Dietary components provide nutrients for bacteria, which produce metabolites involved in energy balance, metabolism and immune response. The interplay between poor diet and dysbiosis changes the metabolism
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