S Torri

Gliclazide protects human islet beta-cells from apoptosis induced by intermittent high glucose.

Decreased beta‐cell mass, mainly due to apoptosis, is crucial for the development and progression of type 2 diabetes. Chronic exposure to high glucose levels is a probable underlying mechanism, whereas the role of oral anti‐diabetic agents (sulphonylureas in particular) is still unsettled.

NO-glibenclamide derivatives: Prototypes of a new class of nitric oxide-releasing anti-diabetic drugs

Endothelial dysfunction and consequent reduction of biosynthesis of endogenous nitric oxide (NO) play an important pathogenetic role in the cardiovascular complications associated with type II diabetes. In this work, the hybrid drugs 3a and 3b, nitrooxymethylbenzoate-derivatives of 1 (which is a hydroxylated active metabolite of glibenclamide 2), are reported. The pharmacodynamic characterization of 3b showed that its hypoglycaemic activity is enriched with additional NO-donor effects, conferring vasorelaxing and anti-platelet properties of potentially great usefulness for diabetes-related cardiovascular disorders.

Effects of C-peptide on isolated human pancreatic islet cells

Recent data have demonstrated that pro‐insulin‐derived C‐peptide can affect the function of several different cell types. We hypothesized that C‐peptide might have an influence on the function and survival of isolated human islets.