Nanocellulose Prepared from Buckwheat Bran: Physicochemical Characterization, Cytotoxicity Evaluation, and Inhibition Effect on Fat Digestion and Absorption.

Cellulose nanocrystal (CNC) is a sustainable biomaterial that has been used in many aspects of the food industry, but its effect on fat digestion and absorption is still underexplored. In this study, three CNCs were prepared from buckwheat bran. Their physicochemical properties were characterized, based on which the acetic acid-hydrolyzed CNC (ACCNC) with high absorption capacity was selected for the cytotoxicity evaluation and as a possible inhibitor for fat digestion and absorption in vitro and in vivo. ACCNC was proved to be nontoxic in the MTT assay and animal feeding tests. Especially, with the addition of ACCNC, the hydrolysis of fat was significantly reduced during the simulated digestion in vitro. In vivo testing also confirmed that ACCNC intake significantly reduced the elevated triglyceride, body weight, and fat accumulation levels. This study highlights the potential role of ACCNC prepared from buckwheat bran as an inhibitor for fat digestion and absorption.

Ferulic Acid Prevents Nonalcoholic Fatty Liver Disease by Promoting Fatty Acid Oxidation and Energy Expenditure in C57BL/6 Mice Fed a High-Fat Diet.

There is a consensus that ferulic acid (FA), the most prominent phenolic acid in whole grains, displays a protective effect in non-alcoholic fatty liver disease (NAFLD), though its underlying mechanism not fully elucidated. This study aimed to investigate the protective effect of FA on high-fat diet (HFD)-induced NAFLD in mice and its potential mechanism. C57BL/6 mice were divided into the control diet (CON) group, the HFD group, and the treatment (HFD+FA) group, fed with an HFD and FA (100 mg/kg/day) by oral gavage for 12 weeks. Hematoxylin and eosin (H&E) staining and Oil Red O staining were used to evaluate liver tissue pathological changes and lipid accumulation respectively. It was demonstrated that FA supplementation prevented HFD-induced NAFLD, which was evidenced by the decreased accumulation of lipid and hepatic steatosis in the HFD+FA group. Specifically, FA supplementation decreased hepatic triacylglycerol (TG) content by 33.5% (p < 0.01). Metabolic cage studies reveal that FA-treated mice have elevated energy expenditure by 11.5% during dark phases. Mechanistically, FA treatment increases the expression of rate-limiting enzymes of fatty acid oxidation and ketone body biosynthesis CPT1A, ACOX1 and HMGCS2, which are the peroxisome proliferator-activated receptors α (PPARα) targets in liver. In conclusion, FA could effectively prevent HFD-induced NAFLD possibly by activating PPARα to increase energy expenditure and decrease the accumulation of triacylglycerol in the liver.