Two Laminaria japonica polysaccharides with distinct structure characterization affect gut microbiota and metabolites in hyperlipidemic mice differently.

Our previous study found dietary mannogluconic acid (MA) and fucogalactan sulfate (FS) from Laminaria japonica have distinct structure characterization and potential hypolipidemic effects in vitro. Herein, we compared the benefits of MA and FS on hyperlipidemia. The result showed only FS treatment decreased body weight and serum cholesterol levels. Compared with MA, FS was more effective in mitigating hepatic fat accumulation, promoting GSH-Px activity, reducing the MDA formation, and lowering the level of TNF-α in liver. Gut microbiota and metabolism analysis revealed that FS increased the relative abundance of beneficial bacteria and boosted the level of short chain fatty acids. Particularly, taurine and 3α,7α,12α-trihydroxy-24-oxo-5-ß-cholestanoyl CoA were upregulated by FS, which might attribute to the increased Oscillibacter and thus affect the enterohepatic circulation of bile acids and serum TC level. Therefore, FS with more branches and sulfate ester groups could be a good lipid-lowering dietary supplement.

In Vitro Digestion and Fermentation of Three Polysaccharide Fractions from Laminaria japonica and Their Impact on Lipid Metabolism-Associated Human Gut Microbiota.

Our previous study has proved that the three polysaccharide fractions from L. japonica (LP-A4, LP-A6, and LP-A8) had significantly different structure characterization. Herein, we conducted in vitro simulated digestion and fermentation to study the digestive mechanism of LP-As. The results of gastrointestinal digestion indicated that LP-A6 and LP-A8 would be easier to trap the enzyme molecules for their denser interconnected macromolecule network compared with LP-A4. Fermentation of LP-As by human gut microbiota, especially for LP-A8, generated a large amount of short-chain fatty acids (SCFAs), which could upregulate the abundance of Firmicutes ( Lachnoclostridium and Eubacterium). The high content of sulfate and highly branched sugar residue of LP-A8 might help it be easily used by Firmicutes in gut microbiota of hyperlipidemic patients. Functional analysis revealed that the increased metabolic activities of glycerophospholipid metabolism, ether lipid metabolism, and fatty acid metabolism induced by LP-A8 treatment were closely associated with metabolic syndromes and hyperlipidemia.

Chicken breast muscle hydrolysates ameliorate acute alcohol-induced liver injury in mice through alcohol dehydrogenase (ADH) activation and oxidative stress reduction.

In this study, the ameliorative effect of chicken breast muscle hydrolysates (CBMHs) against acute alcohol-induced liver injury was investigated and its probable mechanism was further elucidated. In vitro studies clearly showed that CBMHs are able to activate alcohol metabolic enzymes (i.e. alcohol dehydrogenase, ADH) in an exponential manner. Meanwhile, an in vivo experiment on male NIH mice indicated that the oral administration of CBMHs (150, 300 and 600 mg per kg bw) 30 min prior to acute alcohol ingestion could significantly promote alcohol metabolism as revealed by the reduced duration of the loss of righting reflex (LORR) and the enhanced activity of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) in the liver, the latter accelerating alcohol oxidation and therefore the decreased blood alcohol concentration (BAC) level. Pretreatment with CBMHs significantly decreased the elevations of serum aspartate transaminase (AST) and alanine transaminase (ALT) after alcohol administration. CBMHs could also retard lipid peroxidation as revealed by the suppressed malondialdehyde (MDA) level and simultaneously enhance the activities of superoxide dismutase (SOD) in liver tissue. Furthermore, increased histological damage and higher (p < 0.05) hepatic triglyceride (TG) contents in acute alcoholic-diet fed mice were also reduced (p < 0.05) by supplementing with CBMHs. These benefits clearly suggested that CBMHs could be a potential nutraceutical to facilitate alcohol metabolism and prevent or ameliorate early liver injury induced by acute alcohol exposure.