Gut microbial fatty acid metabolites (KetoA and KetoC) affect the progression of nonalcoholic steatohepatitis and reverse cholesterol transport metabolism in mouse model
Autor: | Shigenobu Kishino, Jiawen Zheng, Tatsuya Sugawara, Neng Tanty Sofyana, Yuki Manabe, Yuta Yamamoto, Jun Ogawa |
---|---|
Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Male medicine.medical_specialty medicine.disease_cause Diet High-Fat Biochemistry Streptozocin 03 medical and health sciences chemistry.chemical_compound Liver disease Mice Non-alcoholic Fatty Liver Disease Internal medicine medicine Animals Humans Gene Regulatory Networks chemistry.chemical_classification 030109 nutrition & dietetics biology Bacteria Cholesterol Gene Expression Profiling Organic Chemistry Reverse cholesterol transport Cholesterol HDL Fatty acid Cell Biology Metabolism Hep G2 Cells biology.organism_classification medicine.disease Lactic acid Gastrointestinal Microbiome Disease Models Animal Oxidative Stress 030104 developmental biology Endocrinology chemistry Gene Expression Regulation Linoleic Acids Disease Progression Oxidative stress |
Zdroj: | LipidsReferences. 55(2) |
ISSN: | 1558-9307 |
Popis: | Nonalcoholic steatohepatitis (NASH) is a common liver disease that occurs in both alcoholics and nonalcoholics. Oxidative stress is a possible causative factor for liver diseases including NASH. Gut microorganisms, especially lactic acid bacteria, can produce unique fatty acids, including hydroxy, oxo, conjugated, and partially saturated fatty acids. The oxo fatty acid 10-oxo-11(E)-octadecenoic acid (KetoC) provides potent cytoprotective effects against oxidative stress through activation of Nrf2-ARE pathway. The aim of this study was to explore the preventive and therapeutic effects of gut microbial fatty acid metabolites in a NASH mouse model. The mice were divided into 3 experimental groups and fed as follows: (1) high-fat diet (HFD) (2) HFD mixed with 0.1% KetoA (10-oxo-12(Z)-octadecenoic acid), and (3) HFD mixed with 0.1% KetoC. After 3 weeks of feeding, plasma parameters, liver histology, and mRNA expression of multiple genes were assessed. There was hardly any difference in fat accumulation in the histological study; however, no ballooning occurred in 2/5 mice of KetoC group. Bridging fibrosis was not observed in the KetoA group, although KetoA administration did not significantly suppress fibrosis score (p = 0.10). In addition, KetoC increased the expression level of HDL related genes and HDL cholesterol levels in the plasma. These results indicated that KetoA and KetoC may partly affect the progression of NASH in mice models. |
Databáze: | OpenAIRE |
Externí odkaz: |