Beneficial effects of molasses extract in treatment of nonalcoholic fatty liver disease in high-fat diet-induced obese rats through regulation of lipid metabolism, bile acid, and oxidative stress
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Abstract
Background
One useful byproduct of the sugar industry is molasses. Main phytochemicals consist of phenolic compounds, plant sterols, octacosanol, tocopherol, and policosanol, which have antioxidant and hypolipidemic properties, reduce oxidative stress and inflammation. A natural product extracted from molasses, which has not been previously evaluated in context, was investigated for the treatment of nonalcoholic fatty liver disease (NAFLD) in high-fat diet-induced obese rats, thus contributing new evidence for therapeutic approaches to NAFLD.
Methods
The rats were divided into five groups: a control group, a high-fat diet (HFD) group, two groups receiving a low dose (M250) or a high dose (M400) of molasses extract, as well as a positive control group (P20). After four weeks on the high-fat diet, the rats were treated with oral administration of the substance. This study investigated parameters associated with obesity, NAFLD, oxidative markers, lipid metabolism, bile acid pathways, and liver morphological changes.
Results
Molasses extract significantly improved lipid profiles, increased expression of nuclear factor erythroid 2-related factor 2 protein, resulting in elevated antioxidant enzyme activities and reduced malondialdehyde levels, improved lipid and bile acid metabolisms by enhancing the expressions of low-density lipoprotein receptor, cholesterol 7-alpha-monooxygenase, bile salt export pump, and β-oxidation markers. The extract downregulated the expression of fatty acid synthase, acetyl-CoA carboxylase, HMG-CoA reductase, and cluster of differentiation 36. The histopathological results showed a notable reduction in NAS scores.
Conclusions
Molasses extract showed promising therapeutic effects against NAFLD in obese rats, improving hepatic steatosis, antioxidant defenses, and modulating lipid metabolism and bile acid pathways.