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Propionate alleviates high‐fat diet‐induced lipid dysmetabolism by modulating gut microbiota in mice
Author(s) -
Song B.,
Zhong Y.Z.,
Zheng C.B.,
Li F.N.,
Duan Y.H.,
Deng J.P.
Publication year - 2019
Publication title -
journal of applied microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.889
H-Index - 156
eISSN - 1365-2672
pISSN - 1364-5072
DOI - 10.1111/jam.14389
Subject(s) - sodium propionate , endocrinology , medicine , propionate , gut flora , white adipose tissue , adipocyte , adipose tissue , sodium butyrate , lipid metabolism , biology , chemistry , biochemistry , gene
Aims The aims were to examine whether oral sodium propionate supplementation regulate lipid metabolism through modulating gut microbiota. Methods and Results ICR male mice (26·98 ± 0·30 g) were randomly assigned to three groups ( n = 10) and fed control diet (Con), high‐fat diet (HFD) and HFD plus propionate (Pro) respectively. In this study, we found that HFD increased the weight of final body, inguinal white adipose tissues (iWAT), epididymal white adipose tissue (eWAT) and perirenal white adipose tissue (pWAT), as well as the adipocyte mean area of iWAT and eWAT in mice ( P < 0·05), whereas sodium propionate treatment reduced the weight of iWAT and pWAT as well as adipocyte mean area of iWAT in mice fed a HFD ( P < 0·05). Moreover, in the iWAT, the mRNA expression of lipogenesis genes, including peroxisome proliferator activated receptor γ, acetyl‐CoA carboxylase and carnitine palmitoyl transferase‐1β, was upregulated by HFD challenge ( P < 0·05), and the elevation of these genes was nearly reversed to the level of control diet‐fed mice by sodium propionate treatment. Meanwhile, sodium propionate treatment increased the hormone‐sensitive lipase mRNA expression in the iWAT of HFD‐fed mice ( P < 0·05). High‐throughput pyrosequencing of the 16S rRNA demonstrated that sodium propionate treatment significantly recovered the gut microbiota dysbiosis in HFD‐fed mice, including the richness and diversity of microbiota and the ratio of Firmicutes to Bacteroidetes. Furthermore, the HFD‐induced reductions in colonic levels of butyrate and valerate were reversed by sodium propionate treatment, which also normalized the serum LPS level seen in HFD‐fed mice to the levels of the control diet‐fed mice. Conclusions Collectively, these results indicated that sodium propionate treatment could improve lipid metabolism in HFD‐fed mice, and the potential mechanisms might be via regulating gut microbiota. Significance and Impact of the Study We demonstrated for the first time that oral sodium propionate significantly improved HFD‐induced dysbiosis of gut microbiota, indicating that the mitigative effect of propionate for HFD‐induced lipid dysmetabolism might be mediated by gut microbiota in mice.