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. 2024 Jan 23;12(2):231.
doi: 10.3390/microorganisms12020231.

Novel Wild-Type Pediococcus and Lactiplantibacillus Strains as Probiotic Candidates to Manage Obesity-Associated Insulin Resistance

Affiliations

Novel Wild-Type Pediococcus and Lactiplantibacillus Strains as Probiotic Candidates to Manage Obesity-Associated Insulin Resistance

Paraskevi Somalou et al. Microorganisms. .

Abstract

As the food and pharmaceutical industry is continuously seeking new probiotic strains with unique health properties, the aim of the present study was to determine the impact of short-term dietary intervention with novel wild-type strains, isolated from various sources, on high-fat diet (HFD)-induced insulin resistance. Initially, the strains were evaluated in vitro for their ability to survive in simulated gastrointestinal (GI) conditions, for adhesion to Caco-2 cells, for bile salt hydrolase secretion, for cholesterol-lowering and cellular cholesterol-binding ability, and for growth inhibition of food-borne pathogens. In addition, safety criteria were assessed, including hemolytic activity and susceptibility to antibiotics. The in vivo test on insulin resistance showed that mice receiving the HFD supplemented with Pediococcus acidilactici SK (isolated from human feces) or P. acidilactici OLS3-1 strain (isolated from olive fruit) exhibited significantly improved insulin resistance compared to HFD-fed mice or to the normal diet (ND)-fed group.

Keywords: Lactiplantibacillus; Pediococcus; high-fat diet; insulin resistance; obesity; probiotics; type2 diabetes.

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Conflict of interest statement

Author Panayiotis Panas was employed by QLCon. The remaining 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
Analysis of cholesterol binding by the different bacterial strains. Binding of cholesterol was analyzed by flow cytometry using the green fluorescent CholEsteryl BODIPYTM FL C12. Bacteria were treated with CholEsteryl for 15 h. Only PI-negative, live cells were analyzed. Positive cells for CholEsteryl (FITC+) were evaluated based on untreated controls analyzed for each strain. (a) Representative flow cytometry graphs showing the gating strategy. (b) Representative flow cytometry density plots of untreated control bacteria (Control) and bacteria treated with CholEsteryl (CholEsteryl). (c) Representative density plots of at least two individual experiments illustrating the cholesterol-binding capacity for the different bacterial strains analyzed. Data were analyzed with FlowJo (v.10, Ashland, OR, USA).
Figure 2
Figure 2
Glucose tolerance test in mice that received (A) normal diet, ND, high-fat diet, HFD, and HFD supplemented with P. acidilactici SK, (B) ND, HFD, and HFD supplemented with P. acidilactici OLL1-1, (C) ND, HFD, and HFD supplemented with P. acidilactici OLS2-1, (D) ND, HFD, and HFD supplemented with Lb. plantarum SK4, (E) ND, HFD, and HFD supplemented with P. acidilactici OLS3-1,(F) ND, HFD, and HFD supplemented with Lb. pentosus PE11, and (G) ND, HFD, and HFD supplemented with Lb. plantarum RS1. * p< 0.05, ** p< 0.01, *** p< 0.001, ND versus HFD, ## p< 0.01, ### p< 0.001, ND versus HFD + potential probiotic, $ p< 0.05, $$ p< 0.01 HFD versus HFD + potential probiotic.
Figure 3
Figure 3
Fecal microbial populations in mice fed (A) normal diet, ND, high-fat diet, HFD, and HFD supplemented with P. acidilactici SK (HFD + SK), Lb. plantarum SK4 (HFD + SK4), and P. acidilactici OLL1-1 (HFD + OLL1-1), and (B) ND, HFD, and HFD supplemented with P. acidilactici OLS2-1 (HFD + OLS2-1), P. acidilactici OLS3-1 (HFD + OLS3-1), Lb. pentosus PE11 (HFD + PE11), and Lb. plantarum RS1 (HFD + RS1).

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