Gut micobiota alteration by Lactobacillus rhamnosus reduces pro-inflammatory cytokines and glucose level in the adult model of Zebrafish

Objective Type 2 diabetes mellitus (T2DM) is still a challenge for physicians to manage patient’s circumstances. It is assumed that alterations in the normal flora may be involved in the pathogenesis of T2DM through inducing chronic inflammation. To investigate the effect of Lactobacillus rhamnosus...

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Published in:BMC research notes 2021-08, Vol.14 (1), p.1-302, Article 302
Main Authors: Bootorabi, Fatemeh, Saadat, Farshid, Falak, Reza, Manouchehri, Hamed, Changizi, Reza, Mohammadi, Hasan, Safavifar, Farnaz, Khorramizadeh, Mohammad Reza
Format: Article
Language:English
Subjects:
Acclimation
Biometrics
Body mass index
Cytokine
Cytokines
Diabetes
Diabetes mellitus (non-insulin dependent)
Glucose
Inflammation
Insulin resistance
Lactobacillus rhamnosus
Metabolism
Metabolites
Microbiota
Obesity
Pathogenesis
Probiotic
Probiotics
Research Note
Statistical analysis
Type 2 diabetes mellitus (T2DM)
Zebrafish
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Summary:Objective Type 2 diabetes mellitus (T2DM) is still a challenge for physicians to manage patient’s circumstances. It is assumed that alterations in the normal flora may be involved in the pathogenesis of T2DM through inducing chronic inflammation. To investigate the effect of Lactobacillus rhamnosus as a common probiotic on T2DM, we induced an experimental model of T2DM in adult male Zebrafish by gradient hyper-glucose accumulation methodology. Results In this trial 3-month old male adult Zebrafish were divided in to four groups including two control groups and T2DM induced groups with or without probiotic treatment. After 5 days of acclimation, T2DM was induced by a gradient hyper-glucose accumulation methodology. Diabetic fishes had statistically abnormal blood glucose and pro-inflammatory cytokine levels compared to control group (p = 0.0001). These results suggest that probiotic intervention decreased the blood glucose level in the T2DM-P group by decreasing pro-inflammatory cytokines responsible for signaling in T2DM therapeutic modalities.
ISSN:1756-0500
1756-0500
DOI:10.1186/s13104-021-05706-5