Impaired glucose tolerance results from Cr restriction in animals, and Cr supplementation improves glucose tolerance in diabetic animals. These effects are presumably due to the role of Cr in glucose tolerance factor (GTF), a complex of Cr and nicotinic acid believed to facilitate insulin binding. Humans, however, do not uniformly respond to Cr supplementation. The present study was designed to evaluate the possibility that the failure results from inadequate levels of dietary nicotinic acid to serve as substrate for GTF synthesis. Sixteen healthy elderly volunteers were divided into three groups and given either 200 micrograms Cr, 100 mg nicotinic acid, or 200 micrograms Cr + 100 mg nicotinic acid daily for 28 days and evaluated on days 0 and 28. Fasting glucose and glucose tolerance were unaffected by either chromium or nicotinic acid alone. In contrast, the combined chromium-nicotinic acid supplement caused a 15% decrease in a glucose area integrated total (p less than .025) and a 7% decrease in fasting glucose. None of the treatments exerted any effect on fasting or one-hour insulin levels. Thus, these data suggest that the inability to respond to chromium supplementation may result from suboptimal levels of dietary nicotinic acid.