The predicted mechanisms and evidence of probiotics on type 2 diabetes mellitus (T2DM)

Abstract

Type 2 diabetes mellitus (T2DM) is a serious endocrine and metabolic disease that is highly prevalent and causes high mortality and morbidity rates worldwide. This review aims to focus on the potential of probiotics in the management of T2DM and its complications and to summarise the various mechanisms of action of probiotics with respect to T2DM. In this review, experimental studies conducted between 2016 and 2022 were explored. The possible mechanisms of action are based on their ability to modulate the gut microbiota, boost the production of short-chain fatty acids (SCFAs) and glucagon-like peptides, inhibit α-glucosidase, elevate sirtuin 1 (SIRT1) levels while reducing fetuin-A levels, and regulate the level of inflammatory cytokines. This review recommends carrying out further studies, especially human trials, to provide robust evidence-based knowledge on the use of probiotics for the treatment of T2DM.

IMPACT STATEMENT

• T2DM is prevalent worldwide causing high rates of morbidity and mortality.

• Gut microbiota play a significant role in the pathogenesis of T2DM.

• Probiotics can be used as possible therapeutic tools for the management of T2DM.

• The possible mechanisms of action of probiotics include modulation of the gut microbiota, production of SCFAs and glucagon-like peptides, inhibition of α-glucosidase, raising SIRT1, reducing fetuin-A levels, and regulating the level of inflammatory cytokines.

Keywords:

• Probiotics
• type 2 diabetes mellitus
• gut microbiota
• inflammations

Author contributions

OB and KSD designed and draft the initial manuscript and wrote the paper, LS, IC and YT critically reviewed and revised the manuscript. All the authors have approved the final version to be submitted.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

Data sharing not applicable to this article as no data sets were generated or analysed during the current study

Additional information

Funding

The authors declare that there has been no support received before the writing of this review.