Effect of nicotinamide treatment on the residual insulin secretion in Type 1 (insulin-dependent) diabetic patients
In vivo and in vitro experiments have shown that nicotinamide enhances the regeneration of rat B cells. Nicotinamide has been administered to human subjects at a dose of 3 g/day for more than one year without any serious side effects. A trial was conducted to study if nicotinamide could protect B cells in Type I (insulin-dependent) diabetic patients with established diabetes, but still with residual insulin secretion, the latter being evaluated throughout the study period. A randomized double-blind study was carried out on 26 Type I diabetic patients aged 15 to 40 years who had been treated with insulin for 1 to 5 years but who had a residual insulin secretion characterized by a glucagon stimulated C-peptide level higher than 0.1 nmol/l. They were given either 3 g/day of nicotinamide or a placebo for nine months. At baseline the treated and control groups did not differ according to age, diabetes duration, insulin dose, HbA1c or C-peptide levels. Three patients dropped out of the study. At 9 months there were no significant changes in the insulin doses required. However, HbA1c rose in the control group (8.1±0.4 vs 9.8±0.5%, p<0.05) but not in the nicotinamide treated group (7.5±0.5 vs 6.9±0.4%). Insulin secretion deteriorated in the control patients (fasting C-peptide: 0.28±0.05 vs 0.12±0.03 nmol/l, p<0.05; post glucagon C-peptide: 0.34±0.07vs 0.14±0.02, p<0.05) but not in the treated patients (fasting C-peptide: 0.22±0.04 vs 0.24±0.05 nmol/l; post glucagon C-peptide: 0.30±0.04 vs 0.33±0.07). At six and nine months, fasting and stimulated C-peptide were higher in the treated than in the non-treated group. The C-peptide response to a meal test gradually declined in the placebo group, whereas it was stable in the nicotinamide treated group. No serious side effects were noted; in particular, hepatic function and plasma lipid content remained unchanged. These results suggest that nicotinamide treatment may protect residual B-cell function in Type 1 diabetes; but further studies are needed to assess the clinical implications of such treatment.