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, the less effectively insulin reduces fat release from fat cells, the less effectively niacin does too, suggesting both substances are affected by the same underlying problem in how fat breakdown is controlled.

In healthy, lean individuals, insulin reduces the breakdown of fat in both fat tissue and muscle, and muscle tissue requires less insulin to achieve this effect than fat tissue.

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.

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.

In people with obesity or type 2 diabetes, the way their bodies respond to insulin and niacin in suppressing free fatty acids varies from person to person, but those who do not respond well to one of these agents typically also do not respond well to the other.