Nicotinic acid increases adipose tissue dietary fatty acid trapping and reduces postprandial hepatic and cardiac fatty acid uptake in prediabetes.

Increased adipose tissue (AT) dietary fatty acids (DFA) trapping limits fatty acid exposure to lean organs in the face of elevated postprandial nonesterified fatty acid (NEFA) flux from excess AT intracellular lipolysis in prediabetes. We hypothesized that pharmacological inhibition of postprandial AT intracellular lipolysis using short-acting nicotinic acid (NA) would increase AT DFA trapping and limit AT NEFA spillover to lean organs in subjects with prediabetes. Twenty subjects with impaired glucose tolerance and 19 individuals with normal glucose tolerance underwent four postprandial studies with positron emission tomography/computed tomography with radio-labeled fatty acid tracers and stable isotopic palmitate tracers. Over the 6-h postprandial period, NA increased AT DFA partitioning with reciprocal reduction in liver and in muscle. NA also robustly reduced cardiac and liver total (DFA + NEFA) postprandial fatty acid uptake. Short-acting NA administered postprandially thus enhances AT DFA trapping and markedly reduces postprandial hepatic and cardiac fatty acid uptake. (clinicaltrials.gov NCT02808182).