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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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Detalles Bibliográficos
Autores principales: Bootorabi, Fatemeh, Saadat, Farshid, Falak, Reza, Manouchehri, Hamed, Changizi, Reza, Mohammadi, Hasan, Safavifar, Farnaz, Khorramizadeh, Mohammad Reza
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8351095/
https://www.ncbi.nlm.nih.gov/pubmed/34372916
http://dx.doi.org/10.1186/s13104-021-05706-5
Descripción
Sumario: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. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13104-021-05706-5.