Cited by 131Gut microbiota and healthProbiotics and Fermented FoodsDiabetes and associated disorders

Probiotics and prebiotics for the amelioration of type 1 diabetes: Present and future perspectives

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Mishra, Sidharth, Wang, Shaohua, Nagpal, Ravinder, Miller, Brandi, Singh, Ria, Taraphder, Subhash, Yadav, Hariom·2019·Microorganisms

Abstract

Type 1-diabetes (T1D) is an autoimmune disease characterized by immune-mediated destruction of pancreatic beta (β)-cells. Genetic and environmental interactions play an important role in immune system malfunction by priming an aggressive adaptive immune response against β-cells. The microbes inhabiting the human intestine closely interact with the enteric mucosal immune system. Gut microbiota colonization and immune system maturation occur in parallel during early years of life; hence, perturbations in the gut microbiota can impair the functions of immune cells and vice-versa. Abnormal gut microbiota perturbations (dysbiosis) are often detected in T1D subjects, particularly those diagnosed as multiple-autoantibody-positive as a result of an aggressive and adverse immunoresponse. The pathogenesis of T1D involves activation of self-reactive T-cells, resulting in the destruction of β-cells by CD8+ T-lymphocytes. It is also becoming clear that gut microbes interact closely with T-cells. The amelioration of gut dysbiosis using specific probiotics and prebiotics has been found to be associated with decline in the autoimmune response (with diminished inflammation) and gut integrity (through increased expression of tight-junction proteins in the intestinal epithelium). This review discusses the potential interactions between gut microbiota and immune mechanisms that are involved in the progression of T1D and contemplates the potential effects and prospects of gut microbiota modulators, including probiotic and prebiotic interventions, in the amelioration of T1D pathology, in both human and animal models.

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  • Probiotics diminish inflammatory, autoimmune, and oxidative stress responses.

    “Furthermore, probiotics diminish the inflammatory, autoimmune, and OS responses.”

    From A critical review on diabetes mellitus type 1 and type 2 management approaches: from lifestyle modification to current and novel targets and therapeutic agents. (2024) · cites this paper as [107]

    Section 3.1 (Animal Studies; page unavailable) reports that probiotic-fermented milk decreased inflammation and oxidative stress in rats. Sections 3.1 and 3.2 discuss reduced intestinal inflammation and associations with lower β-cell autoimmunity, but the evidence concerns particular strains and settings, and the human autoimmunity finding is hedged. The unqualified claim that probiotics diminish all three responses overstates the review. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Probiotics from Bifidobacteria and Lactobacilli taken orally showed encouraging antidiabetic effects.

    “Probiotics from Bifidobacteria (including Bifidobacterium infantis, Bifidobacterium longum, and Bifidobacterium breve) and Lactobacilli (including Lactobacillus acidophilus, Lactiplantibacillus plantarum, Lactobacillus bulgaricus, and Lactobacillus delbrueckii subsp. that were taken orally showed encouraging antidiabetic effects.”

    From A critical review on diabetes mellitus type 1 and type 2 management approaches: from lifestyle modification to current and novel targets and therapeutic agents. (2024) · cites this paper as [107]

    Section 3.1 (Animal Studies; no page given) reports beneficial effects of fed Lactobacillus strains and Bifidobacterium-containing probiotics in diabetic mice and rats. That supports the broad claim, but the paper does not substantiate antidiabetic effects for most of the specific species listed in the citing sentence; the evidence cited here is chiefly from animal studies. (LLM, conf=0.85)

    Experimental — accuracy not yet measured
  • Probiotics may boost incretins, decrease endoplasmic reticulum stress, decrease systemic lipopolysaccharide levels, improve peripheral insulin sensitivity, and preserve the integrity of the gut.

    “Probiotics may boost incretins, decrease endoplasmic reticulum stress, decrease systemic lipopolysaccharide levels, improve peripheral insulin sensitivity, and preserve the integrity of the gut.”

    From A critical review on diabetes mellitus type 1 and type 2 management approaches: from lifestyle modification to current and novel targets and therapeutic agents. (2024) · cites this paper as [107]

    Section 3 (page unavailable) says probiotics may increase GLP-1, an incretin, and that specific strains help maintain gut membrane integrity and prevent leakiness and endotoxemia. It does not say probiotics decrease endoplasmic reticulum stress or systemic lipopolysaccharide levels. Section 5 (page unavailable) mentions improved insulin sensitivity only for metformin combined with probiotics and/or prebiotics, not probiotics alone. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • Lacticaseibacillus rhamnosus, when mixed with B. lactis and Lactobacillus gasseri, inhibits weight gain in humans, specifically fat tissue mass adiposity.

    “Lacticaseibacillus rhamnosus, when mixed with B. lactis and Lactobacillus gasseri, has been demonstrated to inhibit weight gain in humans, specifically fat tissue mass adiposity, which strengthens the efficacy of probiotics in diabetes (105–107).”

    From A critical review on diabetes mellitus type 1 and type 2 management approaches: from lifestyle modification to current and novel targets and therapeutic agents. (2024) · cites this paper as [107]

    Section 3.2 (Human Studies; page not provided) reports L. rhamnosus GG and B. lactis Bb12 supplementation in children with type 1 diabetes, but describes effects on gut microbiota and immune cells, not weight gain or fat mass. The cited paper does not report a human mixture including L. gasseri or demonstrate the claimed adiposity effect. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

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Cited by

Sorted by citations

Authors
Mishra, S., Wang, S., Nagpal, R., Miller, B., Singh, R., Taraphder, S., & Yadav, H.
Affiliations
  • Wake Forest University Health Sciences (US)
  • West Bengal University of Animal and Fishery Sciences (IN)
Corresponding author
Yadav, Hariom
Venue
Microorganisms
Publisher
MDPI AG
Published
2019-03-02
Volume
7
Issue
3
Pages
67
ISSN
2076-2607 (ISSN-L)
OpenAlex
W2919655320
Cited by
131
References
7
Citations by year
2026: 5 · 2025: 11 · 2024: 24 · 2023: 17 · 2022: 27 · 2021: 24 · 2020: 17 · 2019: 5 · 2018: 1
FWCI
1.61
Type
journal article
Language
en
Open access
Locations
  • Microorganisms (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institutes of Health (UL1TR001420)
  • Congressionally Directed Medical Research Programs (PR170446)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Keywords
type 1 diabetes, probiotics, prebiotics, gut microbiota, dysbiosis, islet autoimmunity, CD8+ T cells, intestinal barrier integrity, tight junction proteins, autoimmune disease, multiple autoantibodies, gut-immune interaction

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