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Garam Yang Department of Biological Sciences, College of Natural Sciences, Chonnam National University, Buk-Gu, Gwangju, Republic of Korea

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Eunjeong Hong Department of Biological Sciences, College of Natural Sciences, Chonnam National University, Buk-Gu, Gwangju, Republic of Korea

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Sejong Oh Division of Animal Science, College of Agriculture & Life Sciences, Chonnam National University, Buk-Gu, Gwangju, Republic of Korea

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Eungseok Kim Department of Biological Sciences, College of Natural Sciences, Chonnam National University, Buk-Gu, Gwangju, Republic of Korea

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We previously reported that Lactobacillus amylovorus KU4 (LKU4) promotes adipocyte browning in mice fed a high-fat diet (HFD mice) in part by remodeling the PPARγ transcription complex. However, the mechanism through which LKU4 enables PPARγ to drive adipocyte browning remains elusive. Here, we report that LKU4 inhibits the expression of PP4C in inguinal white adipose tissue of HFD mice and in insulin-resistant 3T3-L1 adipocytes, which promotes SIRT1-dependent PPARγ deacetylation by activating AMPK, leading to the browning of adipocytes. Consistently, the silencing of PP4C further enhances this pathway. Furthermore, we observed that lactate, a key LKU4 metabolite, reduces insulin-induced PP4C expression and suppresses PP4C inhibition of PPARγ deacetylation and transcriptional activity via AMPK–SIRT1, thereby facilitating the browning of adipocytes. Together, these data demonstrate that LKU4 promotes the AMPK–SIRT1–PPARγ pathway by inhibiting PP4C, thereby facilitating adipocyte browning in HFD mice.

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Sung-Soo Park Department of Biological Sciences, College of Natural Sciences, Chonnam National University, Gwangju, South Korea

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Yeon-Joo Lee Department of Biological Sciences, College of Natural Sciences, Chonnam National University, Gwangju, South Korea

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Sooyeon Song Division of Animal Science, College of Agriculture & Life Science, Chonnam National University, Gwangju, South Korea

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Boyong Kim Gwangju Center, Korea Basic Science Institute, Gwangju, South Korea

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Hyuno Kang Gwangju Center, Korea Basic Science Institute, Gwangju, South Korea

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Sejong Oh Division of Animal Science, College of Agriculture & Life Science, Chonnam National University, Gwangju, South Korea

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Eungseok Kim Department of Biological Sciences, College of Natural Sciences, Chonnam National University, Gwangju, South Korea

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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.

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