ABSTRACT
Protecting pancreatic β-cells from metabolic insults, preserving the ability of β-cells to secrete insulin and preventing ß-cell exhaustion constitute a therapeutic strategy to prevent metabolic syndrome. Metabolic syndrome encompasses hyperglycemia and insulin resistance, which can lead to type 2 diabetes in genetically predisposed individuals. Once insulin resistance is in full blown, β-cells in the pancreas need to secrete more insulin in an attempt to decrease glycemia, and increased postprandial glycemia constitutes a status of "glucotoxicity" for pancreatic β-cell leading to the generation of reactive oxygen species and ultimately type 2 diabetes. An interesting characteristic of Stephania tetrandra S. Moore is that contains bisbenzyl-isoquinoline alkaloids with the ability to protect β-cells in rodents. Streptozotocin is produced by Streptomyces achromogenes and causes in experimental animals irreversible destruction of β-cells. Evidence is accumulating that the fruits of Cucurbita ficifolia Bouche contains natural product(s) the oral administration of which decrease glycemia in diabetic rodents via increased insulin secretion by remaining functional β-cells.
