Lactobacillus amylovorus KU4 ameliorates diet-induced obesity in mice by promoting adipose browning through PPARγ signaling

Park, Sung Soo; Lee, Yeon Joo; Kang, Hyeonggon; Yang, Garam; Hong, Eun Jeong; Lim, Jin Yeong; Oh, Sejong; Kim, Eungseok

doi:10.1038/s41598-019-56817-w

Cited by 40 publications

(36 citation statements)

References 30 publications

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“…This interest extends to the improvement of various inflammatory diseases. Particularly, probiotic treatment is an effective and safe approach to reversing metabolic abnormalities observed not only in obesity [28,29], but also in NAFLD [30]. In this study, treatment with two L. plantarum strains, K2 and K6, improved HF/HF diet-induced NAFLD in rats by regulating liver function, serum lipid levels, and lipogenesis via the AMPK pathway.…”

Section: Discussionmentioning

confidence: 76%

Beneficial Effects of Lactobacillus plantarum Strains on Non-Alcoholic Fatty Liver Disease in High Fat/High Fructose Diet-Fed Rats

et al. 2020

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Emerging evidence suggests that probiotics are beneficial in non-alcoholic fatty liver disease (NAFLD). This study aimed to explore the effects of two Lactobacillus plantarum strains, ATG-K2 and ATG-K6 (isolated from Korean fermented cabbage), in a rat model of high fat/high fructose (HF/HF) diet-induced NAFLD. Rats with NAFLD were randomized into four groups (HF/HF diet control, (HC); HF/HF diet with silymarin, (PC); HF/HF diet with ATG-K2, (K2); and HF/HF diet with ATG-K6, (K6)) with healthy rats on a normal diet serving as the negative control. After treatment, histopathological and biochemical analyses of the blood and liver tissue were conducted. In addition, fecal microbiota was analyzed using the MiSeq platform. Compared with HC rats, K2 and K6 rats experienced significantly lower body weight gain, displayed decreased hepatic lipid accumulation, had lower serum levels of aspartate aminotransferase and alanine aminotransferase, and showed increased antioxidant enzyme activities. Moreover, de novo lipogenesis-related genes were downregulated following K2 and K6 administration. The fecal microbiota of K2 and K6 rats contained a higher proportion of Bacteriodetes and a lower proportion of Fimicutes than that of HC rats. Taken together, our results suggest that L. plantarum strains ATG-K2 and ATG-K6 are potential therapeutic agents for NAFLD.Nutrients 2020, 12, 542 2 of 16 of the transcription factors, such as sterol regulatory element binding protein 1c (SREBP-1c) and CCAAT/enhancer-binding protein alpha (C/EBPα), which in turn regulate the expression of hepatic gluconeogenesis and DNL genes [6]. It follows that fructose intake increases liver gluconeogenesis and DNL and elevates blood glucose and TG levels in humans [8,9] Another cause of NAFLD is oxidative stress. Fat deposition occurring in the liver results in lipid peroxidation, and it promotes a variety of responses such as inflammation and fibrosis. Thus, antioxidants (e.g., silymarin, vitamin E) are proposed as candidates for NAFLD treatment [10,11]; however, there are no standard pharmacological therapeutic agents for NAFLD yet. Recently, emerging evidence suggests that the gut-liver axis is strongly related to NAFLD. There are several reports published clinical trials applying probiotics on NAFLD patients [12]. Lactobacillus bulgaricus and Streptococcus thermophiles treatment improved liver aminotransferases levels in adult NAFLD patients [13]. In addition, probiotic capsules containing Lactobacillus acidophilus, Bifidobacterium lactis, Bifidobacterium bifidum, and Lactobacillus rhamnosus, as a supplement also decreased liver aminotransferases levels in obese children with NAFLD [14]. These results indicate that the intake of certain probiotics has a beneficial effect on NAFLD.Lactobacillus plantarum, which plays a key role in the production of various fermented foods, is one of the most important species of lactic acid bacteria (LAB). L. plantarum is found in diverse environments, such as the soil and the human gut, and is considered a potential pro...

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Section: Discussionmentioning

confidence: 76%

Beneficial Effects of Lactobacillus plantarum Strains on Non-Alcoholic Fatty Liver Disease in High Fat/High Fructose Diet-Fed Rats

et al. 2020

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“…Recent studies in mice and human volunteers showed that several strains of probiotic bacteria, such as Lactobacillus acidophilus NS1, Lactobacillus amylovorus KU4, and Akkermansia muciniphila , ameliorate obesity and associated metabolic disorders [ 3 , 4 , 17 ]. To determine whether NV probiotic bacteria have a similar effect on the reduction of diet-induced obesity, 7-week-old male mice were fed HFD with or without oral administration of NV-LJ3402 for 14 weeks.…”

Section: Resultsmentioning

confidence: 99%

“…In addition, NV-LJ3402-CM was added to HEK293T cells for 24 h to test its effect on the activities of transcription factors. Adipocyte differentiation of 3T3-L1 cells and transfections were performed as previously described [ 4 ].…”

Section: Methodsmentioning

confidence: 99%

“…Total RNA was isolated from 3T3-L1 cells and WATs using Trizol reagent (Invitrogen, Waltham, MA, USA), and cDNA was synthesized from 1 μg total RNA using Moloney Murine Leukemia Virus (M-MLV)Reverse Transcriptase (Promega, Madison, WIS, USA). Real time-quantitative PCR (RT-qPCR) was performed as previously described [ 4 ], and the results were normalized to 36B4 mRNA expression. Relative quantification of PCR products was calculated by the difference in Ct values between the target and 36B4 genes using the 2 −ΔΔCt method.…”

Section: Methodsmentioning

confidence: 99%

“…Lactobacillus acidophilus NS1 inhibits obesity in high-fat diet (HFD)-fed mice by increasing hepatic fatty acid oxidation with decreased lipogenesis, improving HFD-induced insulin resistance, nonalcoholic fatty liver disease, and hyperlipidemia [ 3 ]. In addition, another Lactobacillus strain, Lactobacillus amylovorus KU4, promotes the browning of WAT in HFD-fed mice, leading to the suppression of HFD-induced adiposity with reduced lipid deposition in metabolic tissues, such as liver and WAT as well as improved insulin sensitivity [ 4 ]. The World Health Organization and the Food and Agriculture Organization of the United Nations define probiotics as living beneficial microorganisms [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

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Non-Viable Lactobacillus johnsonii JNU3402 Protects against Diet-Induced Obesity

Yang

Hong

et al. 2020

Foods

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In this study, the role of non-viable Lactobacillus johnsonii JNU3402 (NV-LJ3402) in diet-induced obesity was investigated in mice fed a high-fat diet (HFD). To determine whether NV-LJ3402 exhibits a protective effect against diet-induced obesity, 7-week-old male C57BL/6J mice were fed a normal diet, an HFD, or an HFD with NV-LJ3402 for 14 weeks. NV-LJ3402 administration was associated with a significant reduction in body weight gain and in liver, epididymal, and inguinal white adipose tissue (WAT) and brown adipose tissue weight in HFD-fed mice. Concomitantly, NV-LJ3402 administration to HFD-fed mice also decreased the triglyceride levels in the plasma and metabolic tissues and slightly improved insulin resistance. Furthermore, NV-LJ3402 enhanced gene programming for energy dissipation in the WATs of HFD-fed mice as well as in 3T3-L1 adipocytes with increased peroxisome proliferator-activated receptor-γ (PPARγ) transcriptional activity, suggesting that the PPARγ pathway plays a key role in mediating the anti-obesity effect of NV-LJ3402 in HFD-fed mice. Furthermore, NV-LJ3402 administration in HFD-fed mice enhanced mitochondrial levels and function in WATs and also increased the body temperature upon cold exposure. Together, these results suggest that NV-LJ3402 could be safely used to develop dairy products that ameliorate diet-induced obesity and hyperlipidemia.

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The PKA‐SREBP1c Pathway Plays a Key Role in the Protective Effects of Lactobacillus johnsonii JNU3402 Against Diet‐Induced Fatty Liver in Mice

Hong,

Kang,

Yang

et al. 2023

Molecular Nutrition Food Res

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ScopeThe present study aims to assess the protective effect of Lactobacillus johnsonii JNU3402 (LJ3402) against diet‐induced non‐alcoholic fatty liver disease (NAFLD) and determine the mechanism underlying its beneficial effect on the liver in mice.Methods and resultsSeven‐week‐old male mice are fed a high‐fat diet (HFD) with or without oral supplementation of LJ3402 for 14 weeks. In mice fed an HFD, LJ3402 administration alleviates liver steatosis, diet‐induced obesity, and insulin resistance with a decreased hepatic expression of sterol‐regulatory element‐binding protein‐1c (SREBP‐1c), fatty acid synthase (FAS) and acetyl‐CoA carboxylase (ACC), and an increased phosphorylation of SREBP‐1c. The mechanistic study shows that LJ3402 inhibits SREBP‐1c transcriptional activity by enhancing protein kinase A (PKA)‐mediated phosphorylation and reduces the expression of its lipogenic target genes in AML12 and HepG2 cells, thereby attenuating hepatic lipid accumulation. Moreover, silencing the PKA α catalytic subunit or the inhibition of PKA activity by H89 abolishes LJ3402 suppression of free fatty acid (FFA)‐induced SREBP‐1c activity in hepatocytes. In addition, LJ3402 administration elevates the plasma lactate levels in mice fed an HFD; this lactate increases PKA‐mediated SREBP‐1c phosphorylation in AML12 cells with a decreased expression of its target genes, reducing hepatic lipid accumulation.ConclusionLJ3402 attenuates HFD‐induced fatty liver in mice through the lactate‐PKA‐SREBP‐1c pathway.

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Lactobacillus amylovorus KU4 ameliorates diet-induced obesity in mice by promoting adipose browning through PPARγ signaling

Cited by 40 publications

References 30 publications

Beneficial Effects of Lactobacillus plantarum Strains on Non-Alcoholic Fatty Liver Disease in High Fat/High Fructose Diet-Fed Rats

Beneficial Effects of Lactobacillus plantarum Strains on Non-Alcoholic Fatty Liver Disease in High Fat/High Fructose Diet-Fed Rats

Non-Viable Lactobacillus johnsonii JNU3402 Protects against Diet-Induced Obesity

The PKA‐SREBP1c Pathway Plays a Key Role in the Protective Effects of Lactobacillus johnsonii JNU3402 Against Diet‐Induced Fatty Liver in Mice

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