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Cited by 142Probiotics and Fermented FoodsGut microbiota and healthMicrobial Metabolites in Food Biotechnology

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Probiotics as Complementary Treatment for Metabolic Disorders

Open access
Le Barz, Mélanie, Anhê, Fernando F., Varin, Thibaut V., Desjardins, Yves, Levy, Emile, Roy, Denis, Urdaci, Maria C., Marette, André·2015·Diabetes & Metabolism Journal
DOI 10.4093/dmj.2015.39.4.291PMC PMC4543192
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Abstract

Recent studies have demonstrated beneficial effects of specific probiotics on alleviating obesity-related disorders.Here we aimed to identify probiotics with potential antiobesity activity among 88 lactic acid bacterial strains via in vitro screening assays, and a Lactobacillus plantarum strain K21 was found to harbor abilities required for hydrolyzing bile salt, reducing cholesterol, and inhibiting the accumulation of lipid in 3T3-L1 preadipocytes.Furthermore, effects of K21 on diet-induced obese (DIO) mice were examined.Male C57Bl/6J mice received a normal diet, high-fat diet (HFD), or HFD with K21 administration (10 9 CFU in 0.2 mL PBS/day) for eight weeks.Supplementation of K21, but not placebo, appeared to alleviate body weight gain and epididymal fat mass accumulation, reduce plasma leptin levels, decrease cholesterol and triglyceride levels, and mitigate liver damage in DIO mice.Moreover, the hepatic expression of peroxisome proliferator-activated receptor-𝛾 (PPAR-𝛾) related to adipogenesis was significantly downregulated in DIO mice by K21 intervention.We also found that K21 supplementation strengthens intestinal permeability and modulates the amount of Lactobacillus spp., Bifidobacterium spp., and Clostridium perfringens in the cecal contents of DIO mice.In conclusion, our results suggest that dietary intake of K21 protects against the onset of HFD-induced obesity through multiple mechanisms of action.

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Fig. 1 Potential beneficial effects of probiotic supplementation against metabolic disorders. GPR, G protein-coupled receptor; SCFA, short-chain fatty acid; ChREBP, carbohydrate-responsive element-binding protein; SREBP, sterol regulatory element-binding protein; AMPK, AMP-activated protein kinase; ANGPTL4, angiopoietin-like protein 4; TJ, tight junction; AJ, adherens junction.
Fig. 1 Potential beneficial effects of probiotic supplementation against metabolic disorders. GPR, G protein-coupled receptor; SCFA, short-chain fatty acid; ChREBP, carbohydrate-responsive element-binding protein; SREBP, sterol regulatory element-binding protein; AMPK, AMP-activated protein kinase; ANGPTL4, angiopoietin-like protein 4; TJ, tight junction; AJ, adherens junction.CC BY-NC · PubMed Central
Fig. 2 Potential direct effects of probiotics to protect gut microbiota and intestinal barrier integrity. Obesogenic diet or "Western diet" alter gut microbiota population diversity and intestinal barrier integrity. Cross-talk between ingested probiotics, gut microbiota (commensal bacteria) and epithelial cells (1). Probiotics produce metabolites that could serve to increase both the diversity of commensal bacteria and the availability of nutrients used by intestinal epithelial cells (IEC). Commensal bacteria multiply and in turn, also produce metabolites that could be used by surrounding cells. In patients suffering from metabolic disorders, intestinal permeability is altered leading to an increase of low-grade inflammation and metabolic endotoxemia (2). Probiotics can increase production of tight- and adherens junction (TJ and AJ) proteins (3), improving gut permeability and inhibiting the passage of lipopolysaccharides (LPS) into systemic circulation that decreases metabolic endotoxemia. Moreover, probiotics express microorganism-associated molecular patterns (MAMPs) that could bind to host pattern recognition receptors (PRRs) located at cell surface of IEC (1) and dendritic cells (4), and induce the activation/inhibition of signaling pathways. For example (5), probiotics can stimulate dendritic cells leading to inhibition of pro-inflammatory CD4+ cell proliferation and activation of anti-inflammatory pathways (Treg and plasma cell proliferation, resulting in production of anti-inflammatory cytokines and IgA immunoglobulins (6), respectively). Mainly present in the mucus layer, IgA reinforce the protective role of mucosal barrier. Mucus production can also be increased by probiotics that stimulate goblet cells leading to activation of mucin gene expression and therefore production of mucin glycoproteins (7). Once assembled, these proteins are excreted and form the mucus layer, which acts as barrier against pathogen colonization. However, probiotics can also induce physical barrier against pathogens or produce bacteriocins that inhibits undesirable microorganism invasion (8). TLR, Toll-like receptor; NLR, NOD-like receptor; TNF-α, tumor necrosis factor α; IFN-γ, interferon γ; TGF-β, transforming growth factor β; IL-10, interleukin 10.
Fig. 2 Potential direct effects of probiotics to protect gut microbiota and intestinal barrier integrity. Obesogenic diet or "Western diet" alter gut microbiota population diversity and intestinal barrier integrity. Cross-talk between ingested probiotics, gut microbiota (commensal bacteria) and epithelial cells (1). Probiotics produce metabolites that could serve to increase both the diversity of commensal bacteria and the availability of nutrients used by intestinal epithelial cells (IEC). Commensal bacteria multiply and in turn, also produce metabolites that could be used by surrounding cells. In patients suffering from metabolic disorders, intestinal permeability is altered leading to an increase of low-grade inflammation and metabolic endotoxemia (2). Probiotics can increase production of tight- and adherens junction (TJ and AJ) proteins (3), improving gut permeability and inhibiting the passage of lipopolysaccharides (LPS) into systemic circulation that decreases metabolic endotoxemia. Moreover, probiotics express microorganism-associated molecular patterns (MAMPs) that could bind to host pattern recognition receptors (PRRs) located at cell surface of IEC (1) and dendritic cells (4), and induce the activation/inhibition of signaling pathways. For example (5), probiotics can stimulate dendritic cells leading to inhibition of pro-inflammatory CD4+ cell proliferation and activation of anti-inflammatory pathways (Treg and plasma cell proliferation, resulting in production of anti-inflammatory cytokines and IgA immunoglobulins (6), respectively). Mainly present in the mucus layer, IgA reinforce the protective role of mucosal barrier. Mucus production can also be increased by probiotics that stimulate goblet cells leading to activation of mucin gene expression and therefore production of mucin glycoproteins (7). Once assembled, these proteins are excreted and form the mucus layer, which acts as barrier against pathogen colonization. However, probiotics can also induce physical barrier against pathogens or produce bacteriocins that inhibits undesirable microorganism invasion (8). TLR, Toll-like receptor; NLR, NOD-like receptor; TNF-α, tumor necrosis factor α; IFN-γ, interferon γ; TGF-β, transforming growth factor β; IL-10, interleukin 10.CC BY-NC · PubMed Central

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Research works printed but not linked: 4

  1. Wu, 2015, Evid Based Complement Alternat Med, 2015, 391767
  2. Hariri, 2015, ARYA Atheroscler, 11, 74
  3. Quevrain, 2015, Gut
  4. Dudonne, 2015, PharmaNutrition

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Metadata

Authors
Le Barz, M., Anhê, F. F., Varin, T. V., Desjardins, Y., Levy, E., Roy, D., Urdaci, M. C., & Marette, A.
Affiliations
  • Department of Medicine, Faculty of Medicine, Cardiology Axis of the Québec Heart and Lung Institute, Québec, QC, Canada.
  • Institut universitaire de cardiologie et de pneumologie de Québec (CA)
  • Université Laval (CA)
  • Centre Hospitalier Universitaire Sainte-Justine (CA)
  • University of Bordeaux, UMR 5248, CBMN, Bordeaux, France.
Corresponding author
Marette, André
ORCID
Venue
Diabetes & Metabolism Journal
Publisher
Korean Diabetes Association
Published
2015
Volume
39
Issue
4
Pages
291
ISSN
  • 2233-6079 (ISSN-L)
  • 2233-6087
DOI
10.4093/dmj.2015.39.4.291
PMC
PMC4543192
OpenAlex
W2167419149
Cited by
142
References
61
Citations by year
2026: 8 · 2025: 18 · 2024: 10 · 2023: 9 · 2022: 14 · 2021: 7 · 2020: 15 · 2019: 14 · 2018: 14 · 2017: 15 · 2016: 15 · 2015: 3
FWCI
2.01
Type
journal article
Language
en
Update notices
erratum (2015-10-22)
Open access
Licence
Locations
  • Diabetes & Metabolism Journal (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Oskar-Bordeaux (Universite de Bordeaux) (submittedVersion)
Topics
  • Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Health Sciences › Nursing › Nutrition and Dietetics › Microbial Metabolites in Food Biotechnology
Keywords
probiotics, Lactobacillus plantarum, anti-obesity, diet-induced obesity, high-fat diet, bile salt hydrolysis, cholesterol lowering, leptin, hepatic steatosis, PPARγ, intestinal permeability, gut microbiota, 3T3-L1 preadipocytes, metabolic disorders

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