Nerve growth factor increases in pancreatic beta cells after streptozotocin-induced damage in rats.

We investigated short-term in vivo and in vitro effects of streptozotocin (STZ) on pancreatic beta cells. Male Wistar rats were treated with 75 mg/kg STZ, and, after 4 hrs blood glucose and insulin were measured and islet cells were isolated, cultured for 16 hrs, and challenged with 5.6 and 15.

Protective effect of testosterone on early apoptotic damage induced by streptozotocin in rat pancreas.

Beta-cell apoptosis is responsible for the development of insulin-dependent diabetes mellitus in the streptozotocin (STZ) rat model. It has been demonstrated that steroid hormones possess antioxidant and protective antiapoptotic effects in many tissues. The aim of the present study was to investigate the early apoptotic damage induced by STZ in rat pancreas, and the effect of testosterone in preventing apoptosis of pancreatic beta cells.

Ultrastructural changes in pancreatic beta cells treated with NGF and dbcAMP.

Nerve growth factor (NGF) induces morphological and physiological changes in cultured pancreatic beta-cells, including the extension of neurite-like processes. This latter effect is potentiated by dibutyryl cAMP (dbcAMP). beta-cells cultured under these conditions maintain their immunoreactivity to insulin and gamma-amino-butyric acid (GABA).

Heterogeneity in glutamic acid decarboxylase expression among single rat pancreatic beta cells.

Aims/hypothesis: An isoform of glutamic acid decarboxylase, (GAD)65 has been identified as a pancreatic beta-cell autoantigen in Type I (insulin dependent) diabetes mellitus. We investigated the expression of GAD isoforms among single rat beta cells in culture, under different conditions and the correlation between GAD65 expression and insulin secretion-rate.

Results: Independent of culture conditions, 100 % of fresh and cultured beta cells express GAD67.

Insulinotropic action of alpha-D-glucose pentaacetate: functional aspects.

The functional determinants of the insulinotropic action of alpha-D-glucose pentaacetate were investigated in rat pancreatic islets. The ester mimicked the effect of nutrient secretagogues by recruiting individual B cells into an active secretory state, stimulating proinsulin biosynthesis, inhibiting 86Rb outflow, and augmenting 45Ca efflux from prelabeled islets. The secretory response to the ester was suppressed in the absence of Ca2+ and potentiated by theophylline or cytochalasin B.