# Antidiabetic Effects of Anthocyanins on Pancreatic β-Cell Function: A Systematic Review of In Vitro Studies

**Authors:** Ravish Kumkum, Theresha Ruwan Pathiranage, Bryony A. McNeill, Leni R. Rivera, Kathryn Aston-Mourney

PMC · DOI: 10.3390/ijms27031415 · International Journal of Molecular Sciences · 2026-01-30

## TL;DR

This review explores how anthocyanins, found in berries, may protect pancreatic β-cells in type 2 diabetes by reducing stress and improving insulin function in lab studies.

## Contribution

The study systematically reviews in vitro evidence showing anthocyanins' protective effects on β-cells and identifies key molecular mechanisms involved.

## Key findings

- Anthocyanins improved β-cell viability and reduced apoptosis and oxidative stress in various cell models.
- They enhanced insulin secretion and modulated pathways like MAPK signaling and ER stress responses.
- Higher concentrations than typically found in the blood were needed for these effects in vitro.

## Abstract

Pancreatic β-cell dysfunction is the key driver of type 2 diabetes, and anthocyanins have been proposed as dietary compounds that may help preserve β-cell health. This systematic review aimed to synthesise evidence on the direct effects of anthocyanins on β-cell viability, apoptosis, oxidative stress, and insulin secretion across in vitro models. Four databases were searched in March–April 2025, and eighteen studies met the inclusion criteria. Purified anthocyanins—including cyanidin-3-glucoside (C3G), cyanidin-3-rutinoside (C3R), malvidin-3-glucoside (M3G), and delphinidin-3-glucoside (D3G)—as well as anthocyanin-rich berry extracts, were tested in INS-1, MIN6, RIN-m5F cells and primary mouse or human islets under glucotoxic, lipotoxic, oxidative, cytokine, and amyloidogenic stress. Anthocyanins consistently improved β-cell viability, reduced apoptosis, and lowered reactive oxygen species (ROS), nitric oxide (NO), and thiobarbituric acid reactive substances (TBARSs) levels while enhancing antioxidant enzyme activities. Multiple studies showed upregulation of insulin secretion-related genes and proteins, and both acute and chronic treatments increased glucose-stimulated insulin secretion under normal and stressed conditions. Mechanistic pathways involved modulation of mitogen-activated protein kinase (MAPK) signalling, endoplasmic reticulum (ER) stress responses, inflammatory mediators, and mitophagy (PINK1/PARKIN). While effective in vitro concentrations were higher than typical circulating levels, the collective evidence highlights anthocyanins as promising β-cell protective agents and underscores the need for studies examining their metabolites and physiologically relevant exposure.

## Linked entities

- **Proteins:** PINK1 (PTEN induced kinase 1), park (parkin)
- **Chemicals:** anthocyanins (PubChem CID 145858)
- **Diseases:** type 2 diabetes (MONDO:0005148)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Pink1 (PTEN induced kinase 1) [NCBI Gene 298575]
- **Diseases:** type 2 diabetes (MESH:D003924), inflammatory (MESH:D007249)
- **Chemicals:** NO (MESH:D009569), M3G (MESH:C458419), C3G (MESH:C462279), TBARSs (MESH:D017392), Anthocyanins (MESH:D000872), glucose (MESH:D005947), ROS (MESH:D017382), C3R (MESH:C428983), D3G (MESH:C494120)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12898225/full.md

## References

73 references — full list in the complete paper: https://tomesphere.com/paper/PMC12898225/full.md

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Source: https://tomesphere.com/paper/PMC12898225