par Sandler, S;Hellerström, Claes;Eizirik, Decio L. 
Référence The Journal of clinical endocrinology and metabolism, 77, 6, page (1574-1576)
Publication Publié, 1993
Référence The Journal of clinical endocrinology and metabolism, 77, 6, page (1574-1576)
Publication Publié, 1993
Article révisé par les pairs
| Résumé : | Nicotinamide currently attracts considerable interest as a compound that might prevent the development of human insulin-dependent diabetes mellitus. The present study investigated the direct actions of nicotinamide on human pancreatic beta-cells. For this purpose, islets were isolated from 11 adult cadaveric donors. The human islets were subsequently precultured in RPMI-1640 (5.6 mmol/L glucose) and 10% fetal calf serum for 3-4 days. The islets were cultured for another 6 days in the same medium in either the presence or absence of 10 mmol/L nicotinamide, and subsequently, islet function was examined. After culture, both groups of islets contained similar amounts of DNA, and DNA synthesis, determined by the tritiated thymidine incorporation rate, was unchanged. The insulin content both on a per islet basis and per DNA was similar in both groups as was the islet glucose oxidation rate. Insulin accumulation into the culture medium was sustained over the entire culture period and did not differ at any time point between the nicotinamide and the control group. Nicotinamide affected neither basal and glucose-stimulated insulin secretion nor (pro)insulin and total protein biosynthesis rates after culture. The insulin response to glucose of the human islets was about 5-fold. In conclusion, the present study shows that nicotinamide does not directly affect human beta-cell function or the cell replicatory rate. This would suggest that any potential beneficial effects observed after treatment with nicotinamide in patients with insulin-dependent diabetes mellitus may not necessarily reflect an action at the beta-cell level. |
