Pharmacologically Active Phytomolecules Isolated from Traditional Antidiabetic Plants and Their Therapeutic Role for the Management of Diabetes Mellitus

Abstract

Diabetes mellitus is a chronic complication that affects people of all ages. The increased prevalence of diabetes worldwide has led to the development of several synthetic drugs to tackle this health problem. Such drugs, although effective as antihyperglycemic agents, are accompanied by various side effects, costly, and inaccessible to the majority of people living in underdeveloped countries. Medicinal plants have been used traditionally throughout the ages to treat various ailments due to their availability and safe nature. Medicinal plants are a rich source of phytochemicals that possess several health benefits. As diabetes continues to become prevalent, health care practitioners are considering plant-based medicines as a potential source of antidiabetic drugs due to their high potency and fewer side effects. To better understand the mechanism of action of medicinal plants, their active phytoconstituents are being isolated and investigated thoroughly. In this review article, we have focused on pharmacologically active phytomolecules isolated from medicinal plants presenting antidiabetic activity and the role they play in the treatment and management of diabetes. These natural compounds may represent as good candidates for a novel therapeutic approach and/or effective and alternative therapies for diabetes.

Keywords: diabetes; medicinal plants; pharmacology; phytoconstituents; traditional medicine.

Figure 1

Flavonoids exerting antidiabetic activity via different mechanistic pathways: Flavonoids increase insulin secretion and improve β-cell function via the PI3K/AKT signaling pathway; increase GLUT-4 translocation through AMPK activation to increase glucose uptake in adipose tissues and skeletal muscles; activate PPAR-γ expression to decrease insulin resistance; activate cAMP/PKA pathway to reduce blood glucose levels and improve glucose tolerance; increase glutathione peroxidase activity to reduce HbA1c levels; decrease G-6-Pase, PEPCK, glycogen phosphorylase, fructose 1,6-biphosphatase and DPP-IV activity in liver to decrease gluconeogenesis, glycogenolysis, and glycoslysis; inhibit SGLT pathway in kidney to decrease renal glucose reabsorption; inhibit GLUT-2, α-amylase and α-glucosidase activity to decrease glucose absorption in the small intestine.