Prebiotic inulin consumption reduces dioxin-like PCB 126-mediated hepatotoxicity and gut dysbiosis in hyperlipidemic Ldlr deficient mice
Autor: | Michael C. Petriello, Jessie B. Hoffman, Chunyan Wang, Yipeng Sui, Changcheng Zhou, Andrew J. Morris, Bernhard Hennig, Pan Deng, M. Abdul Mottaleb |
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Rok vydání: | 2019 |
Předmět: |
Male
medicine.medical_specialty 010504 meteorology & atmospheric sciences Health Toxicology and Mutagenesis medicine.medical_treatment Inulin 010501 environmental sciences Gut flora Toxicology Dioxins 01 natural sciences Article Impaired glucose tolerance chemistry.chemical_compound Mice Internal medicine RNA Ribosomal 16S medicine Animals Glycolysis 0105 earth and related environmental sciences biology Cholesterol Prebiotic General Medicine medicine.disease biology.organism_classification Pollution Polychlorinated Biphenyls Gastrointestinal Microbiome Endocrinology Prebiotics chemistry LDL receptor Dysbiosis Steatosis Chemical and Drug Induced Liver Injury |
Zdroj: | Environ Pollut |
ISSN: | 1873-6424 |
Popis: | Exposure to some environmental pollutants increases the risk of developing inflammatory disorders such as steatosis and cardiometabolic diseases. Diets high in fermentable fibers such as inulin can modulate the gut microbiota and lessen the severity of pro-inflammatory diseases, especially in individuals with elevated circulating cholesterol. Thus, we aimed to test the hypothesis that hyperlipidemic mice fed a diet enriched with 8% inulin would be protected from the pro-inflammatory toxic effects of PCB 126. Four groups of male Ldlr(−/−) mice were fed a high cholesterol diet containing 8% inulin or 8% cellulose (control) for 12 weeks. At weeks 2 and 4, mice were exposed to PCB 126 or vehicle (control). PCB 126 exposure induced wasting and impaired glucose tolerance, which were attenuated by inulin consumption. PCB 126 exposure induced hepatic lipid accumulation and increased inflammatory gene expression, which were both decreased by inulin consumption. In addition, inulin feeding decreased atherosclerotic lesion development in the aortic root and modulated the expression of enzymes related to glycolysis. Finally, 16S rRNA sequencing of gut microbial populations showed that PCB 126 modulated multiple microbiota genera (e.g., 3-fold decrease in Allobaculum and 3-fold increase in Coprococcus) which were normalized in inulin fed mice. Overall our data support the hypothesis that a dietary intervention that targets the gut microbiota may be an effective means of attenuating dioxin-like pollutant-mediated diseases. MAIN FINDING: Dietary inulin protected against PCB 126 induced inflammation, atherosclerosis, and dysbiosis. |
Databáze: | OpenAIRE |
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