Bentong ginger oleoresin mitigates liver injury and modulates gut microbiota in mouse with nonalcoholic fatty liver disease induced by high‐fat diet

Abstract

The present study aimed to examine the protective effect of Bentong ginger oleoresin (BGO) on the occurrence of nonalcoholic fatty liver disease (NAFLD) and its underlying mechanism. In the present study, 14-week BGO treatment reduced the high-fat diet (HFD)-induced obesity. The serum total cholesterol (TC) was reduced from 4.76 ± 0.30 to 3.542 ± 0.49 mmol/L and fatty liver score decreased to the normal level (1.6 ± 0.55). BGO had antihypercholesterolemia activity, alleviated abnormal lipid metabolism, and improved liver fat accumulation. In addition, liver inflammatory cytokine tests and Western blotting analysis indicated that BGO might play an anti-inflammatory role by mediating the NF-κB signaling pathway. Moreover, BGO regulated the gut microbiota in NAFLD mice and finally mediated their benefits for the host, which might be associated with reduced abundance of Lachnospiraceae_NK4A136_group and Fournierella. BGO showed effective liver protection and regulation of gut microbiota for the HFD-induced NAFLD in obese mice. As a result, BGO may serve as an effective dietary supplement for the improvement of NAFLD-related metabolic diseases.

The Molecular Mechanism of Hepatic Lipid Metabolism Disorder Caused by NaAsO2 through Regulating the ERK/PPAR Signaling Pathway

“…PPAR α is the main regulator of liver β- oxidation and microsomal ω oxidation, and CPT-1 is its downstream gene [ 37 ]. In the study of nonalcoholic fatty liver, it has been found that inhibiting the expression of PPAR α and its downstream genes in the liver could reduce the β -oxidation of fatty acids and promote the accumulation of fatty acids in the liver [ 38 , 39 ]. The in vivo experiment of this study found that the expression of the PPAR α gene was lower in the NaAsO 2 group than in the control group, which indicated that NaAsO 2 inhibited the β- oxidation of fatty acids in hepatocytes and promoted the accumulation of lipids in the liver [ 40 , 41 ].…”

The lipid-lowering effects of fenugreek gum, hawthorn pectin, and burdock inulin

“…Lachnospiraceae_NK4A136_group, a distinguishing feature of gut dysbiosis, had higher levels in rats or mice with diseases such as type 2 diabetes, colitis, and NAFLD ( 81–84 ). Thus to decrease the relative abundance of Lachnospiraceae_NK4A136_group might be the key to slowing the development of these diseases ( 81 ).…”

“…Lachnospiraceae_NK4A136_group, a distinguishing feature of gut dysbiosis, had higher levels in rats or mice with diseases such as type 2 diabetes, colitis, and NAFLD ( 81–84 ). Thus to decrease the relative abundance of Lachnospiraceae_NK4A136_group might be the key to slowing the development of these diseases ( 81 ). The level of Lachnospiracea_NK4A136_group, which was strongly related to hyperlipidemia indicators, improved high-fat diet-induced glucose and lipid metabolic disorders ( 85 ).…”

The Positive Effect of 6-Gingerol on High-Fat Diet and Streptozotocin-Induced Prediabetic Mice: Potential Pathways and Underlying Mechanisms

“…Numerous studies have demonstrated the metabolic modulating function of ginger [ 13 , 14 , 24 , 30 ]. Our previous study showed that ginger oleoresin has the function of regulating blood glucose metabolism in mice, and 6G comprises the biggest proportion of active ingredients in ginger oleoresin [ 22 ]. As far as we know, the present work is the first to offer evidence that supplementation with 6G, an active substance in ginger, helps to improve HFD/STZ-induced prediabetes.…”

“…The mice satisfying the prediabetes criteria were randomized into the DC (prediabetic control) group ( n = 8) receiving HFD and 2 other prediabetic groups receiving HFD plus an additional 10 mg/kg·body weight (BW) 6-gingerol ( w / w , HFD+6G, n = 8). During the dosage choice, our prior work was consulted [ 22 ]. Throughout the experiment, food ingestion was documented twice weekly, while body mass was documented on a weekly basis.…”