In people with obesity or type 2 diabetes, insulin and niacin reduce the release of free fatty acids through different early molecular mechanisms, but both ultimately affect the same later regulatory proteins to achieve similar results.

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 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 people with obesity or type 2 diabetes, injecting niacin decreases specific molecular signals in fat tissue that normally help prevent fat breakdown, even though niacin overall reduces fat breakdown.

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.