Research Article Details
| Article ID: | A10092 |
| PMID: | 31491513 |
| Source: | Int J Biol Macromol |
| Title: | MDG-1, an Ophiopogon polysaccharide, restrains process of non-alcoholic fatty liver disease via modulating the gut-liver axis. |
| 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. |
| DOI: | 10.1016/j.ijbiomac.2019.09.007 |
| Strategy ID | Therapy Strategy | Synonyms | Therapy Targets | Therapy Drugs | |
|---|---|---|---|---|---|
| S02 | Enhance lipid metabolism | triglyceride-lowering; lipid tolerance; lipid metabolism | 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) inhibitor; Decreases intestinal cholesterol absorption; FXR agonist; ACC inhibitor; FAS inhibitor; DGAT2 inhibitor; SCD-1 inhibitor | Atorvastatin; Ezetimibe; Obeticholic Acid; GS-9674; GS-0976; TVB-2640; IONIS-DGAT2rx; Aramchol; | Details |
| S05 | Anti-inflammatory | inflammatory | Bile acid; TNF-a inhibitor; Dual PPAR-α and -δ agonists; Toll-Like Receptor; (TLR)-4 antagonist; Caspase inhibitor; ASK-1 inhibitor | Ursodeoxycholic Acid; Pentoxifylline; Elafibranor; JKB-121; Emricasan; Selonsertib; | Details |
| S06 | Regulating intestinal flora | intestine gut microbiota; gut microbiota | farnesoid X receptor (FXR); fibroblast growth factor-19 (FGF19) | Probiotics; Prebiotics; Rifaximin; Yaq-001; Cilofexor; EDP-305; EYP001a; INT-767 | Details |
| S07 | Anti-lipogenesis | de novo lipogenesis; de novo lipogenesis; DNL; anti-lipogenic mechanisms; adipogenesis; anti-obesity | stearoyl-CoA desaturase 1 (SCD-1); Acetyl-coenzyme carboxylase; acyl-CoA carboxylase inhibitor (ACC inhibitor); stearoyl Coenzyme A desaturase inhibitor (SCD inhibitor); THR-beta selective agonist; DGAT2 inhibitor; FASN inhibitor | Aramchol; Firsocostat (GS-0976); VK-2809; ION 224 | Details |
| Diseases ID | DO ID | Disease Name | Definition | Class | |
|---|---|---|---|---|---|
| I14 | 9970 | Obesity | An overnutrition that is characterized by excess body fat, traditionally defined as an elevated ratio of weight to height (specifically 30 kilograms per meter squared), has_material_basis_in a multifactorial etiology related to excess nutrition intake, decreased caloric utilization, and genetic susceptibility, and possibly medications and certain disorders of metabolism, endocrine function, and mental illness. https://en.wikipedia.org/wiki/Obesity | disease of metabolism/acquired metabolic disease/ nutrition disease/overnutrition | Details |