Type 1 diabetes (T1D) is a multifactorial autoimmune disease driven by T-cells against the insulin-producing islet beta-cells, resulting in a marked loss of beta-cell mass and function. Although a genetic predisposal increases susceptibility, the role of epigenetic and environmental factors seems to be much more significant. A dysbiotic gut microbial profile has been associated with T1D patients. Moreover, new evidence propose that perturbation in gut microbiota may influence the T1D onset and progression. One of the prominent features in clinically silent phase before the onset of T1D is the presence of a microbiota characterized by low numbers of commensals butyrate producers, thus negatively influencing the gut permeability. The loss of gut permeability leads to the translocation of microbes and microbial metabolites and could lead to the activation of immune cells. Moreover, microbiota-based therapies to slow down disease progression or reverse T1D have shown promising results. Starting from this evidence, the correction of dysbiosis in early life of genetically susceptible individuals could help in promoting immune tolerance and thus in reducing the autoantibodies production. This review summarizes the associations between gut microbiota and T1D for future therapeutic perspectives and other exciting areas of research.

Del Chierico, F., Rapini, N., Deodati, A., Matteoli, M.c., Cianfarani, S., Putignani, L. (2022). Pathophysiology of Type 1 Diabetes and Gut Microbiota Role. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 23(23), 1-12 [10.3390/ijms232314650].

Pathophysiology of Type 1 Diabetes and Gut Microbiota Role

Rapini, Novella;Deodati, Annalisa;Cianfarani, Stefano;
2022-11-24

Abstract

Type 1 diabetes (T1D) is a multifactorial autoimmune disease driven by T-cells against the insulin-producing islet beta-cells, resulting in a marked loss of beta-cell mass and function. Although a genetic predisposal increases susceptibility, the role of epigenetic and environmental factors seems to be much more significant. A dysbiotic gut microbial profile has been associated with T1D patients. Moreover, new evidence propose that perturbation in gut microbiota may influence the T1D onset and progression. One of the prominent features in clinically silent phase before the onset of T1D is the presence of a microbiota characterized by low numbers of commensals butyrate producers, thus negatively influencing the gut permeability. The loss of gut permeability leads to the translocation of microbes and microbial metabolites and could lead to the activation of immune cells. Moreover, microbiota-based therapies to slow down disease progression or reverse T1D have shown promising results. Starting from this evidence, the correction of dysbiosis in early life of genetically susceptible individuals could help in promoting immune tolerance and thus in reducing the autoantibodies production. This review summarizes the associations between gut microbiota and T1D for future therapeutic perspectives and other exciting areas of research.
24-nov-2022
Pubblicato
Rilevanza internazionale
Recensione
Esperti anonimi
Settore MED/38 - PEDIATRIA GENERALE E SPECIALISTICA
English
butyrate production
dysbiosis
gut microbiome
insulin resistance
intestine permeability
type 1 diabetes (T1D)
Del Chierico, F., Rapini, N., Deodati, A., Matteoli, M.c., Cianfarani, S., Putignani, L. (2022). Pathophysiology of Type 1 Diabetes and Gut Microbiota Role. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 23(23), 1-12 [10.3390/ijms232314650].
Del Chierico, F; Rapini, N; Deodati, A; Matteoli, Mc; Cianfarani, S; Putignani, L
Articolo su rivista
File in questo prodotto:
File Dimensione Formato  
3ijms-23-14650.pdf

accesso aperto

Tipologia: Versione Editoriale (PDF)
Licenza: Creative commons
Dimensione 967.12 kB
Formato Adobe PDF
967.12 kB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/313608
Citazioni
  • ???jsp.display-item.citation.pmc??? 0
  • Scopus 35
  • ???jsp.display-item.citation.isi??? 38
social impact