Nicotinamide and insulin secretion in normal subjects.

Nicotinamide has been given both before and after clinical onset of Type 1 (insulin-dependent) diabetes mellitus in an attempt to prolong beta-cell survival. Nicotinic acid, structurally similar to nicotinamide, induces insulin resistance and increases insulin secretion in healthy individuals. It is not known if nicotinamide has similar effects. Since insulin secretion, as measured by the acute insulin response to intravenous glucose, is used to predict diabetes and to monitor therapy, the effects of nicotinamide must be established before trials in individuals at high risk of progression to Type 1 diabetes can be interpreted. Intravenous tolerance tests were performed according to the ICARUS standard protocol in 10 healthy, adult subjects (age 32 +/- 5.7 years) before and after 14 days of treatment with nicotinamide 25 mg.kg-1.day-1. The acute insulin response after nicotinamide did not differ from the control study, whether measured as the incremental 0-10 min insulin area (278 +/- 142 vs 298 +/- 130 mU.l-1.10 min-1) or as the 1 +/- 3 min insulin level (78 +/- 39 vs 81 +/- 44 mU/l). The late insulin response was equally unaffected, as were basal insulin (5.2 +/- 1.6 vs 5.6 +/- 2.1 mU/l) and glucose (5.0 +/- 0.4 vs 4.9 +/- 0.2 mmol/l) levels and glucose disposal rates (1.98 +/- 0.88 vs 2.04 +/- 0.68%/min). Nicotinamide does not affect insulin secretion and glucose kinetics in normal subjects, confirming its suitability for trials designed to delay or prevent the onset of Type 1 diabetes.