Abstract

Consumption of pectin contributes to changes in the gut microbiota and the metabolism of short-chain fatty acids (SCFAs). We aimed to investigate the effects of and mechanism by which pectin prevented nonalcoholic fatty liver disease (NAFLD) in mice that were fed a high-fat diet containing 30% lard (HF). HF-fed mice that orally ingested pectin for 8 weeks exhibited improvements in lipid metabolism and decreased oxidative stress and inflammation through a mechanism regulated by the mitogen-activated protein kinase pathway. Pectin dose-dependently generated an increase in acetic acid (from 566.4 ± 26.6 to 694.6 ± 35.9 μmol/mL, p < 0.05) and propionic acid (from 474.1 ± 84.3 to 887.0 ± 184.7 μmol/mL, p < 0.05) contents and significantly increased the relative abundance of Bacteroides (from 0.27% to 11.6%), Parabacteroides (from 3.9‰ to 5.3%), Olsenella (from 2.9‰ to 1.3%), and Bifidobacterium (from 0.03% to 1.9%) in the gut of HF-fed mice. Intestinal microbiota and SCFAs may thus contribute to the well-established link between pectin consumption and NAFLD.

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