Plant-Derived Compounds Targeting Pancreatic Beta Cells for the Treatment of Diabetes

Abstract

Diabetes is a global health problem and a national economic burden. Although several antidiabetic drugs are available, the need for novel therapeutic agents with improved efficacy and few side effects remains. Drugs derived from natural compounds are more attractive than synthetic drugs because of their diversity and minimal side effects. This review summarizes the most relevant effects of various plant-derived natural compounds on the functionality of pancreatic beta cells. Published data suggest that natural compounds directly enhance insulin secretion, prevent pancreatic beta cell apoptosis, and modulate pancreatic beta cell differentiation and proliferation. It is essential to continuously investigate natural compounds as sources of novel pharmaceuticals. Therefore, more studies into these compounds' mechanisms of action are warranted for their development as potential anti-diabetics.

Targeting Mitochondrial Calcium Uptake with the Natural Flavonol Kaempferol, to Promote Metabolism/Secretion Coupling in Pancreatic β-cells

“…Kaempferol is a plant-derived compound. Plant products are very attractive molecules to target pancreatic β-cells for the treatment of diabetes [36]. These compounds are more attractive than synthetic drugs because of their diversity and minimal side effects.…”

Quercetin modulates hyperglycemia by improving the pancreatic antioxidant status and enzymes activities linked with glucose metabolism in type 2 diabetes model of rats: In silico studies of molecular interaction of quercetin with hexokinase and catalase

“…The chronic exposure of pancreatic islets cells to ROS reduces insulin gene expression and insulin secretion due to the low level of antioxidant enzymes such as SOD, CAT, and Glutathione peroxidase (GPx) to detoxify free radicals toxicity (Oguri, Motegi, & Endo, 2003;Oyedemi, Yakubu, & Afolayan, 2011). The chronic exposure of pancreatic islets cells to ROS reduces insulin gene expression and insulin secretion due to the low level of antioxidant enzymes such as SOD, CAT, and Glutathione peroxidase (GPx) to detoxify free radicals toxicity (Oguri, Motegi, & Endo, 2003;Oyedemi, Yakubu, & Afolayan, 2011).…”

“…Persistent hyperglycemia remains the primary cause of diabetes complications and oxidative stress resulting from the increased generation of ROS. The chronic exposure of pancreatic islets cells to ROS reduces insulin gene expression and insulin secretion due to the low level of antioxidant enzymes such as SOD, CAT, and Glutathione peroxidase (GPx) to detoxify free radicals toxicity (Oguri, Motegi, & Endo, 2003;Oyedemi, Yakubu, & Afolayan, 2011). SOD is a first-line antioxidant enzyme that catalyzes the dismutation reaction of superoxide anion to oxygen and hydrogen peroxide, which are further detoxified to water and oxygen by the action of CAT.…”

Hypoglycemic potential of Trixis angustifolia aqueous extract in alloxan-induced diabetic mice

“…As far as we know, this is the first work that analyses T. angustifolia hypoglycemic activity. The hypoglycemic activity of T. Data expressed as a mean ± SEM; n = 7 mice/group; a p<0.05: the significant difference with respect to control group; b p<0.05: the significant difference with respect to diabetic group angustifolia aqueous extract at 100 mg/kg may be due to the regeneration of β-cells that were partially destroyed by alloxan, like the effect reported for other plants extracts based on polar solvents (Oh, 2015). A higher hypoglycemic effect at doses >100 mg/kg was expected, but when a dose of 200 mg/kg was administrated a lower reduction in blood glucose levels was observed.…”