Oat-based postbiotics ameliorate high-sucrose induced liver injury and colitis susceptibility by modulating fatty acids metabolism and gut microbiota
J Nutr Biochem. 2023 Dec 24;125:109553. doi: 10.1016/j.jnutbio.2023.109553. Online ahead of print.
ABSTRACT
High-sucrose (HS) consumption leads to metabolic disorders and increases susceptibility to colitis. Postbiotics hold great potentials in combating metabolic diseases and offer advantages in safety and processability, compared with living probiotics. We developed innovative oat-based postbiotics and extensively explored how they could benefit in rats with long-term high-sucrose consumption. The postbiotics fermented with Lactiplantibacillus plantarum (OF-1) and OF-5, the one fermented with the optimal selection of five probiotics (i.e., L. plantarum, Limosilactobacillus reuteri, Lacticaseibacillus rhamnosus, Lactobacillus acidophilus, and Bifidobacterium lactis) alleviated HS induced liver injury, impaired fatty acid metabolism and inflammation through activating AMPK/SREBP-1c pathways. Moreover, oat-based postbiotics restored detrimental effects of HS on fatty acid profiles in liver, as evidenced by the increases in polyunsaturated fatty acids and decreases in saturated fatty acids, with OF-5 showing most pronounced effects. Furthermore, oat-based postbiotics prevented HS exacerbated susceptibility to dextran sodium sulfate caused colitis and reconstructed epithelial tight junction proteins in colons. Oat-based postbiotics, in particular OF-5 notably remodeled gut microbiota composition, e.g., enriching the relative abundances of Akkermansia, Bifidobacterium, Alloprevotella and Prevotella, which may play an important role in the liver-colon axis responsible for improvements of liver functions and reduction of colitis susceptibility. The heat-inactivated probiotics protected against HS-induced liver and colon damage, but such effects were less pronounced compared with oat-based postbiotics. Our findings emphasize the great value of oat-based postbiotics as nutritional therapeutics to combat unhealthy diet induced metabolic dysfunctions.
PMID:38147914 | DOI:10.1016/j.jnutbio.2023.109553