The role of gut microbiota in mediating obesity and diabetes mellitus
D. Pitocco, M. Di Leo, L. Tartaglione, F. De Leva, C. Petruzziello, A. Saviano, A. Pontecorvi, V. Ojetti Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy. dario.pitocco@policlinicogemelli.it
OBJECTIVE: This review inspects the relations between the microbiota and the intestinal immune system in the advancement of metabolic illnesses, such as obesity and diabetes mellitus. The role of the microbiota in intestinal immune defense and the control of metabolism are subject to examination.
MATERIALS AND METHODS: In type 1 diabetes, the adhesion proteins prompt inside the intestinal epithelium prompt a more significant immune response that may result in the destruction of pancreatic β cells by CD8+ T-lymphocytes, as well as increased articulation of interleukin-17, which is associated with autoimmunity. Studies suggest that the beginning of metabolic ailments and certain co-morbidities can be viewed in light of the protection between the gut microbiota and the intestinal immune system. The gut microbiota is analyzed as a key regulator of metabolic ailments. Research demonstrates that obese patients with type 2 diabetes have a certain gut microbiota and that the microbiota is translocated from the gut to the tissues in conjunction with the illness, which instigates inflammation.
RESULTS: Research in animals and people suggests that a probiotic supplement may regulate the gut microbiota, thereby improving the prognosis for diabetes.
CONCLUSIONS: The mechanism underlying this phenomenon relates to a decrease in the inflammatory reaction and oxidative stress, as well as a decrease in leaky gut. Such reactions increase insulin sensitivity and reduce autoimmune responses.
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To cite this article
D. Pitocco, M. Di Leo, L. Tartaglione, F. De Leva, C. Petruzziello, A. Saviano, A. Pontecorvi, V. Ojetti
The role of gut microbiota in mediating obesity and diabetes mellitus
Eur Rev Med Pharmacol Sci
Year: 2020
Vol. 24 - N. 3
Pages: 1548-1562
DOI: 10.26355/eurrev_202002_20213