Abstract
To the Editor.— We read with interest the article by Garg and Grundy 1 in which they convincingly confirmed that nicotinic acid therapy, while greatly improving the lipid profile in patients with NIDDM, caused a marked deterioration in glycemic control. The authors conclude that nicotinic acid should not be used as first-line therapy in patients with NIDDM. The authors suggest that nicotinic acid may cause insulin resistance or enhance hepatic utilization of fatty acids, thereby promoting gluconeogenesis. We would like to suggest that the hyperglycemic effects of nicotinic acid are due to increased circulating nonesterified fatty acid (NEFA) levels caused by the pharmacodynamic effects of the drug. Nicotinic acid has a short suppressive effect on lipolysis and early studies clearly showed that after an early drop in NEFA levels, there was a marked rebound. 2 Glucose levels closely parallel NEFA levels, the NEFAs acting presumably through impaired peripheral glucose oxidation—the Randle
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