Flavonoids for preserving pancreatic beta cell survival and function: A mechanistic review

Although the currently available antidiabetic medications are effective in managing hyperglycemia, vascular complications are common in diabetic patients. Cohort studies have shown preserved beta cell function has a protective role against the development of diabetic complications. Accordingly, beta cell mass and function are important pharmacological targets in the field of diabetes. Growing number of evidence supports the efficacy of flavonoids (e.g., quercetin, kaempferol, luteolin, and epicatechin) for prevention and attenuation of diabetes consequences. The focus of this paper is to give an overview regarding the effects of flavonoids on pancreatic beta cells. Experiments on insulin-releasing cell lines, isolated pancreatic islets, and diabetic animal models have shown that flavonoids strengthen the survival processes and insulin secretory capacity of beta cells. The proposed mechanisms by which flavonoids preserve beta cells survival (against cytokines, glucotoxicity, and lipotoxicity) include inhibition of NF-kappa B signaling, activation of PI3K/Akt pathway, inhibition of nitric oxide generation, and decrease of reactive oxygen species levels. Improving mitochondrial bioenergetic function and stimulating pathways of insulin secretion (e.g., PLC/PKC and/or cAMP/PKA signaling) are mechanisms by which flavonoids improve the secretory capacity of beta cells. These beneficial effects of flavonoids are of great importance because may protect beta cells of diabetic patients before dramatic dysfunction and degeneration.