Lactobacillus acidophilus NS1 attenuates diet-induced obesity and fatty liver

    1. Eungseok Kim1
    1. 1Department of Biological Sciences, College of Natural Sciences, Chonnam National University, Gwangju, South Korea
    2. 2Division of Animal Science, College of Agriculture & Life Science, Chonnam National University, Gwangju, South Korea
    3. 3Gwangju Center, Korea Basic Science Institute, Gwangju, South Korea
    1. Correspondence should be addressed to S Oh or E Kim: soh{at} or ekim{at}


    Obesity is a major threat to public health, and it is strongly associated with insulin resistance and fatty liver disease. Here, we demonstrated that administration of Lactobacillus acidophilus NS1 (LNS1) significantly reduced obesity and hepatic lipid accumulation, with a concomitant improvement in insulin sensitivity, in high-fat diet (HFD)-fed mice. Furthermore, administration of LNS1 inhibited the effect of HFD feeding on the SREBP-1c and PPARα signaling pathways and reduced lipogenesis with an increase in fatty acid oxidation in ex vivo livers from HFD-fed mice. These LNS1 effects were confirmed in HepG2 cells and ex vivo livers by treatment with LNS1 culture supernatant (LNS1-CS). Interestingly, AMPK phosphorylation and activity in the liver of HFD-fed mice were increased by administration of LNS1. Consistently, chemical inhibition of AMPK with compound C, a specific inhibitor of AMPK, dramatically reduced the effect of LNS1-CS on lipid metabolism in HepG2 cells and ex vivo livers by modulating the SREBP-1c and PPARα signaling pathways. Furthermore, administration of LNS1 to HFD-fed mice significantly improved insulin resistance and increased Akt phosphorylation in the liver, white adipose tissue and skeletal muscle. Together, these data suggest that LNS1 may prevent diet-induced obesity and related metabolic disorders by improving lipid metabolism and insulin sensitivity through an AMPK→SREBP-1c/PPARα signaling pathway.

    • Received 13 February 2018
    • Accepted 5 March 2018
    • Made available online as an Accepted Preprint 5 March 2018
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