Co-ordinated Ca(2+)-signalling within pancreatic islets: does beta-cell entrainment require a secreted messenger.

Isolated beta-cells are heterogeneous in sensory, biosynthetic and secretory capabilities, however, to enable efficient and appropriate secretion, cellular activity within the intact islet is synchronised. Historically, the entrainment of activity to a common pattern has been attributed to gap-junction mediated cell-to-cell communication. Although clearly influential, the possibility remains for other local synchronising mechanisms.

Apoptosis and disease progression in the spontaneously diabetic BB/S rat.

Aims/hypothesis: Type I (insulin-dependent) diabetes mellitus is an autoimmune disease culminating in pancreatic beta-cell destruction. A role for apoptosis in this destruction has been suggested, although controversy exists over the identity of the apoptotic cells and the time of onset of apoptosis. This study investigates the extent and timing of islet cell apoptosis in vivo in the spontaneously diabetic BB/S rat.

Glycation of insulin in the islets of Langerhans of normal and diabetic animals.

The glycation of immunoreactive insulin (IRI) was assessed in extracts of pancreas and islets from control and hyperglycemic animal models. Glycated and nonglycated IRI were separated by affinity chromatography and quantified by radioimmunoassay. Hydrocortisone-treated Wistar rats (80 mg x kg-1 x day-1 and obese hyperglycemic (ob/ob) mice showed significant increases in plasma glucose (P < 0.

Effects of okadaic acid on insulin secretion from rat islets of Langerhans.

We have studied the effects of the phosphatase inhibitor, okadaic acid, on insulin secretion and protein phosphorylation in intact and electrically permeabilized pancreatic islets. Okadaic acid inhibited glucose-induced insulin secretion from intact islets, although this effect was probably non-specific since similar effects were obtained using 1-nor-okadaone, a virtually inactive analogue of okadaic acid. In permeabilized islets, okadaic acid enhanced basal and cyclic-AMP-induced insulin secretion and protein phosphorylation.