Corinne Hubinont

Activation of protein kinase C by a tumor-promoting phorbol ester in pancreatic islets

Rat pancreatic islet homogenates display protein kinase C activity. This phospholipid‐dependent and calcium‐sensitive enzyme is activated by diacylglycerol or the tumor‐promoting phorbol ester 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA). In the presence of TPA, the K a for Ca2+ is close to 5 μM. TPA does not affect phosphoinositide turnover but stimulates [32P]‐ and [3H]choline‐labelling of phosphatidylcholine in intact islets. Exogenous phospholipase C stimulates insulin release, in a sustained and glucose‐independent fashion. The secretory response to phospholipase C persists in media deprived of CaCl2. It is proposed that protein kinase C participates in the coupling of stimulus recognition to insulin release evoked by TPA, phospholipase C and, possibly, those secretatogues causing phosphoinositide breakdown in pancreatic islets.

Sorbitol content of plasma and erythrocytes during induced short-term hyperglycemia

Plasma glucose concentration was increased from a mean basal value of 3.3 +/- 0.1 to 13.3 +/- 1.5 mmol/L by the intravenous administration of glucose for 60 minutes to four healthy volunteers. The sorbitol content of erythrocytes was increased during the period of hyperglycemia from a mean basal value of 65 +/- 9 to 106 -/+ 6 mumol/L. The plasma sorbitol concentration remained constant at 12 +/- 1 mumol/L. This dissociated response indicates that the plasma concentration of sorbitol is not significantly affected by a short-term hyperglycemia sufficient to cause intracellular sorbitol accumulation.

Pancreatic islet cell function in oral contraception, pregnancy and lactation - a review

SummaryThe changes in pancreatic B-cell function associated with oral contraception, pregnancy and lactation in either normal or mildly diabetic rats are briefly reviewed. Emphasis is placed on the long-term regulation of B-cell secretory activity by several environmental factors known to be operative in these situations. Such factors may affect not only the activity of key enzymes (e.g. adenylate cyclase and protein kinases) involved in stimulus-secretion coupling, but also the islet content of essential coupling agents (e.g. calcium). The effect of pregnancy and lactation upon islet function appears to be itself modulated by changes in the secretory potential of the endocrine pancreas, such as those resulting from a partial destruction of B-cells by cytotoxic agents.