Berberine-induced glucagon-like peptide-1 and its mechanism for controlling type 2 diabetes mellitus: a comprehensive pathway review

Abstract

Introduction: A growing number of studies have thus far showed the association between type 2 diabetes mellitus (DM) and the intestinal microbiome homoeostasis. As reported, the gut microflora can be significantly different in patients with type 2 DM (T2DM) compared to those in healthy individuals.

Methods: The authors collected the relevant articles published until 2022 and these are carefully selected from three scientific databases based on keywords.

Discussion: This review highlights research on the anti-diabetic properties of berberine (BBR)-induced glucagon-like peptide-1 (GLP-1), as a glucose-lowering factor and a balance regulator in the microbial flora of the intestines, which plays an important role in adjusting the signalling pathways affecting insulin secretion.

Results: Considering the anti-diabetic characteristics of the BBR-induced GLP-1, BBR makes a promising complementary treatment for reducing the clinical symptoms of DM by reducing the hyperglycaemia. Berberin might be a safe and effective drug for T2DM with little or no adverse effects.

Highlights

1. Berberine induces GLP-1 insulin secretion by PLC2 pathway in the intestinal

2. Berberine-induced GLP-1 decreases mitochondrial stress and relocates cytochrome c out of the mitochondria.

3. Berberine induces GLP-1 secretion in the intestine by altering the bacterial profile, thus could possibly lighten diabetes symptoms

4. Berberine-induced SCFA production, SCFA causes GLP-1 secretion from the intestinal L-Cell.

5. Preventing mitochondrial damage, reducing adipose tissue fat, and reducing oxidative stress are thus among the results of BBR-induced GLP-1.

6. The lower costs of BBR, and its limited side effects and higher availability, make it a promising supplementary medicine for DM

Keywords:

• Type 2 diabetes mellitus
• berberine
• glucagon-like peptide-1
• gut microbiota
• intestinal microbiome

Acknowledgements

The authors would like to thank the Aging Research Institute at Tabriz University of Medical Sciences.

Authors’ contributions

Conceptualisation: Mostafa Araj-khodaei, Sarvin Sanaie

Formal analysis: Tannaz Novin Bahador, Ali Shamekh,

Investigation: Tannaz Novin Bahador

Methodology: Ata Mahmoodpoor, Mohammad Hossein Ayati

Project administration: Mostafa Araj-khodaei, Sarvin Sanaie

Resources: Tannaz Novin Bahador, Akbar Azizi Zeinalhajlou

Supervision: Mostafa Araj-khodaei, Sarvin Sanaie

Validation: Nazli Namazi

Writing – review & editing: Tannaz Novin Bahador, Mehdi Yousefi

Ethics approval and consent to participate

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Consent for publication

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Disclosure statement

No potential conflict of interest was reported by the authors.

Availability of data and materials

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