Abstract

MDG-1, a β-D-fructan polysaccharide extracted from the roots of Ophiopogon japonicus, had preventive effect against obesity and hyperlipidemia in high-fat diet (HFD)-induced obesity mice. Interestingly, MDG-1, as an inulin-type fructan, is poorly absorbed and its possible mechanism against lipid disturbance remained unclear. The present study aimed to investigate the benefits of MDG-1 treatment on NAFLD model and elucidate mechanism from the perspective of gut-liver axis, especially about gut microbiota, short chain fatty acids (SCFAs) and hepatic lipid metabolism. In this study, after two months HFD feeding, C57BL/6J male mice were randomly divided into HFD group and various MDG-1 dose group. Results showed that MDG-1 markedly blocked weight gain, and ameliorated lipid accumulation, liver damage and macrovesicular steatosis. MDG-1 could restore gut microbiota balance and increase relative abundance of beneficial bacteria, especially SCFAs-producing bacteria. After degradation and utilization by the gut microbiota, MDG-1 could increase the contents of acetic acid and valeric acid, thus regulating inflammatory responses and hepatic lipid metabolism. Specifically, MDG-1 enhanced expression of hepatic phosphorylation of adenosine monophosphate-activated protein kinase, accompanying by regulating hepatic adipogenesis and adipocyte differentiation, thereby inhibiting progress of NAFLD. Our findings may provide new ways in the treatment of hyperlipidemia and lipid-related metabolic syndrome.

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