Protective effect of triterpenes against diabetes-induced β-cell damage: An overview of in vitro and in vivo studies

Triterpenes display a strong potential to ameliorate diabetes induced β-cell damage through the modulation of several genes and proteins involved in insulin signaling, inflammation, oxidative stress and apoptosis. [Display omitted] Accumulative evidence shows that chronic hyperglycaemia is a major factor implicated in the development of pancreatic β-cell dysfunction in diabetic patients. Furthermore, most of these patients display impaired insulin signalling that is responsible for accelerated pancreatic β-cell damage. Indeed, prominent pathways involved in glucose metabolism such as phosphatidylinositol 3-kinase/ protein kinase B (PI3-K/AKT) and 5′ AMP-activated protein kinase (AMPK) are impaired in an insulin resistant state. The impairment of this pathway is associated with over production of reactive oxygen species and pro-inflammatory factors that supersede pancreatic β-cell damage. Although several antidiabetic drugs can improve β-cell function by modulating key regulators such as PI3-K/AKT and AMPK, evidence of their β-cell regenerative and protective effect is scanty. As a result, there has been continued exploration of novel antidiabetic therapeutics with abundant antioxidant and antiinflammatory properties that are essential in protecting against β-cell damage. Such therapies include triterpenes, which have displayed robust effects to improve glycaemic tolerance, insulin secretion, and pancreatic β-cell function. This review summarises most relevant effects of various triterpenes on improving pancreatic β-cell function in both in vitro and in vivo experimental models. A special focus falls on studies reporting on the ameliorative properties of these compounds against insulin resistance, oxidative stress and inflammation, the well-known factors involved in hyperglycaemia associated tissue damage.