In human fat tissue, neither insulin nor niacin strongly triggers the ERK1/2 signaling pathway under the conditions studied, indicating that this pathway likely does not play a major role in how free fatty acids are taken up by fat cells in the body.

When insulin and niacin reduce fat breakdown to the same degree in healthy individuals, neither causes a greater increase in fat storage under the skin than the other, suggesting that insulin does not uniquely promote fat storage beyond what is expected from reduced fat breakdown.

In people with obesity or type 2 diabetes, niacin still reduces fat breakdown in adipose tissue even when the usual insulin signaling pathways are less active, indicating it may use alternative biological mechanisms to achieve this effect.