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Front Nutr ; 9: 913729, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35990329

RESUMO

Black chokeberry (Aronia melanocarpa L.) is rich in polyphenols with various physiological and pharmacological activities. However, the relationship between the modulation effect of black chokeberry polyphenols on obesity and the alteration of lipid metabolism is not clearly understood. This study aimed to investigate the beneficial effects of the black chokeberry polyphenols (BCPs) treatment on the structure of gut microbiota, lipid metabolism, and associated mechanisms in high-fat diet (HFD)-induced obese rats. Here, we found that a high-fat diet promoted body weight gain and lipid accumulation in rats, while oral BCPs supplementation reduced body weight, liver, and white adipose tissue weight and alleviated dyslipidemia and hepatic steatosis in HFD-induced obese rats. In addition, BCPs supplementation prevented gut microbiota dysbiosis by increasing the relative abundance of Bacteroides, Prevotella, Romboutsia, and Akkermansia and decreasing the relative abundance of Desulfovibrio and Clostridium. Furthermore, 64 lipids were identified as potential lipid biomarkers through lipidomics analysis after BCPs supplementation, especially PE (16:0/22:6), PE (18:0/22:6), PC (20:3/19:0), LysoPE (24:0), LysoPE (24:1), and LysoPC (20:0). Moreover, our studies provided new evidence that composition of gut microbiota was closely related to the alteration of lipid profiles after BCPs supplementation. Additionally, BCPs treatment could ameliorate the disorder of lipid metabolism by regulating the mRNA and protein expression of genes related to the glycerophospholipid metabolism signaling pathway in HFD-induced obese rats. The mRNA and protein expression of PPARα, CPT1α, EPT1, and LCAT were significantly altered after BCPs treatment. In conclusion, the results of this study indicated that BCPs treatment alleviated HFD-induced obesity by modulating the composition and function of gut microbiota and improving the lipid metabolism disorder via the glycerophospholipid metabolism signaling pathway.

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