Enteromorpha prolifera is an edible alga and previous studies have indicated that E. prolifera polysaccharide (EP) attenuates non-alcoholic fatty liver disease (NAFLD) in high-fat diet rats. Hydrogen sulfide (H2S) has recently been found to exert many physiological effects. The purpose of this study was to evaluate whether EP prevents NAFLD via regulation of H2S production. EP was orally administered to high-fat diet rats for 5 weeks. Treatment with EP (200 mg per kg body weight per d) significantly increased the serum H2S level and reduced the serum triglyceride level (p < 0.05) in rats fed a high-fat diet. These effects were similar to those observed with NaHS, a H2S donor. Real-time PCR and western blotting analysis revealed that EP significantly upregulated hepatic mRNA and protein expression of cystathionine-β-synthase, which is the enzyme responsible for H2S production. These results indicate that EP decreases the serum TG level by increasing H2S production, suggesting that EP may be beneficial for the treatment of NAFLD and may reduce the risk of cardiovascular disease.

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Background Obesity-related metabolic diseases have recently evoked worldwide attention. Studies have demonstrated that Enteromorpha polysaccharide (EP) exerts lipid-lowering effects, but the underlying mechanism remains unclear. Objective To investigate whether EP regulates lipid metabolism disorders in mice with high-fat diet (HFD)-induced obesity via an AMP-activated protein kinase (AMPK)-dependent pathway. Methods Six-week-old male C57BL/6J mice (18 ± 2 g) were fed a normal diet (ND; 10% energy from fats) or a HFD (60% energy from fats) for 6 weeks to induce obesity and treated intragastrically with EP (200 mg/kg body weight) or distilled water (10 mL/kg body weight) for 8 weeks. Biochemical indicators, AMPK-dependent pathways and lipid metabolism-related genes were evaluated to assess the effects of EP on HFD-induced lipid metabolism disorders. The essential role of AMPK in the EP-mediated regulation of lipid metabolism was confirmed using HFD-fed male Ampka2-knockout mice (aged 6 weeks, 17 ± 2 g) treated or not treated with the above-mentioned dose of EP. The data were analyzed by t tests and two-factor and one-way ANOVAs. Results Compared to the ND, the HFD resulted in the greater body weight (24.3%), perirenal fat index (2.2-fold), and serum TC (24.66%) and LDL cholesterol (1.25-fold) concentrations (P &lt; 0.05) and dysregulated the AMPK-dependent pathway and the expression of most lipid metabolism-related genes (P &lt; 0.05). Compared to the HFD, EP treatment resulted in the lower perirenal fat index (31.22%) and the LDL-C concentration (23.98%) and partly reversed the dysregulation of the AMPK-dependent pathway and the altered expression of lipid metabolism-related genes (P &lt; 0.05). Ampka2 knockout abolished the above-mentioned effects of EP in obese mice and the EP-mediated effects on the expression of lipid metabolism-related genes (P &gt; 0.05). Conclusions These findings suggest that EP can ameliorate lipid metabolism disorders in mice with HFD-induced obesity via an AMPK-dependent pathway.