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. 2023 Mar 21:80:10794.
doi: 10.3389/bjbs.2023.10794. eCollection 2023.

Faecalibacterium prausnitzii Improves Lipid Metabolism Disorder and Insulin Resistance in Type 2 Diabetic Mice

Wenting Xuan  1 , Yijing Ou  2   3   4 , Wenting Chen  2   3 , Lishan Huang  2   3 , Chuangyu Wen  2   3 , Guangying Huang  1 , Wenting Tang  2   3 , Daidi Zeng  2   3 , Suran Huang  2   3 , Lijuan Xiao  2   3 , Zhongjun Li  2   3   4
Affiliations

Faecalibacterium prausnitzii Improves Lipid Metabolism Disorder and Insulin Resistance in Type 2 Diabetic Mice

Wenting Xuan et al. Br J Biomed Sci. .

Abstract

Purpose: Additional effective therapeutic strategies for Type 2 diabetes (T2D) patients are urgently needed. Gut microbiota plays an important role in T2D development and is a promising treatment strategy for T2D patients. Faecalibacterium prausnitzii (F. prausnitzii) is regarded as one of the most important bacterial indicators for a healthy gut, but the mechanisms of its anti-diabetic properties are still unclear. Methods and Results: The abundance of F. prausnitzii in feces of patients with T2D was detected by using qPCR. The effects of F. prausnitzii on glucose homeostasis, insulin resistance (IR), dyslipidemia, hepatic steatosis and inflammation were investigated in type 2 diabetic (T2D) db/db mice. We also investigated F. prausnitzii in people. Our results showed that the abundance of F. prausnitzii was significantly lower in T2D patients compared to healthy subjects. In T2D mice, we found that F. prausnitzii treatment significantly decreased fasting blood glucose and IR index, indicating improved glucose intolerance as well as IR. Furthermore, based on evaluation of lipid-regulating enzyme activities and proinflammatory cytokine levels, F. prausnitzii was not only able to improve inflammation in both adipose tissue and liver, but also ameliorate hepatic steatosis through inhibiting the activity of hepatic lipogenic enzymes. Conclusion: These results suggested that F. prausnitzii might serve as a therapeutic option for T2D by improved IR, lipid metabolism and inflammation.

Keywords: Faecalibacterium prausnitzii; hepatic steatosis; inflammation; insulin resistance; lipid metabolism; type 2 diabetic.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
The abundance of F. prausnitzii in feces of patients with type-2 diabetes (T2D). (A) The abundance of F. prausnitzii in feces of patients with type-2 diabetes (T2D) and healthy subjects (HS). (B) The abundance of F. prausnitzii in GMrepo T2D cohort. Error bars, SD. ***p < 0.001.
FIGURE 2
FIGURE 2
F. prausnitzii restored insulin resistance of T2D mice. Effect of dietary F. prausnitzii on daily food intake (A), body weight (B), adipose tissue weight (C), blood glucose by IPGTT (D), **p < 0.01, T2D-FP v.s. T2D, HOMA-IR (E) and plasma insulin levels (F) in ND, T2D and T2D-FP mice. Error bars, SD. *p < 0.05, ***p < 0.001.
FIGURE 3
FIGURE 3
F. prausnitzi modulated dyslipidemia and hepatic steatosis of T2D mice. Effect of dietary F. prausnitzii on plasma lipid levels (A), hepatic lipid content (B), hepatic morphology (C), and hepatic lipid-regulating enzyme activity (D) in ND and T2D mice. Error bars, SD. *p < 0.05, **p < 0.01, ***p < 0.001.
FIGURE 4
FIGURE 4
F. prausnitzii attenuated pro-inflammatory cytokine expression in T2D mice. Effect of dietary F. prausnitzii on plasma pro-inflammatory cytokine levels (A), and the mRNA expression of pro-inflammatory cytokines in adipose tissue and livers (B,C) of ND and T2D mice. Error bars, SD. *p < 0.05, **p < 0.01, ***p < 0.001.
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References

    1. Wang Y, Yang L, Yang D, Zhang Q, Deng Z, Wang K, et al. MiR-21 Antagomir Improves Insulin Resistance and Lipid Metabolism Disorder in Streptozotocin-Induced Type 2 Diabetes Mellitus Rats. Ann Palliat Med (2020) 9:394–404. 10.21037/apm.2020.02.28 - DOI - PubMed
    1. Cho N, Shaw J, Karuranga S, Huang Y, da Rocha Fernandes J, Ohlrogge A, et al. IDF Diabetes Atlas: Global Estimates of Diabetes Prevalence for 2017 and Projections for 2045. Diabetes Res Clin Pract (2018) 138:271–81. 10.1016/j.diabres.2018.02.023 - DOI - PubMed
    1. Ma Q, Li Y, Wang M, Tang Z, Wang T, Liu C, et al. Progress in Metabonomics of Type 2 Diabetes Mellitus, 23. Basel, Switzerland: Molecules; (2018). 10.3390/molecules23071834 - DOI - PMC - PubMed
    1. Guerrero-Hernández A, Leon-Aparicio D, Chavez-Reyes J, Olivares-Reyes J, DeJesus S. Endoplasmic Reticulum Stress in Insulin Resistance and Diabetes. Cell calcium (2014) 56:311–22. 10.1016/j.ceca.2014.08.006 - DOI - PubMed
    1. Brown A, Walker M. Genetics of Insulin Resistance and the Metabolic Syndrome. Curr Cardiol Rep (2016) 18:75. 10.1007/s11886-016-0755-4 - DOI - PMC - PubMed