The Claim
In adults with upper-body obesity and/or type 2 diabetes, the suppression of free fatty acid release by insulin and niacin is highly correlated (r = −0.93), indicating that individuals who are resistant to the free fatty acid suppression effect of one agent are almost always resistant to the suppression effect of the other.
What the research says
Supports is higher
Support is ahead, but a single strong opposing study can change this.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
In adults with upper-body obesity or type 2 diabetes, the ability of insulin to reduce free fatty acid release is strongly linked to the ability of niacin to do the same; if one fails to suppress free fatty acids in a person, the other is also unlikely to suppress them.
See the scientific wording
In adults with upper-body obesity and/or type 2 diabetes, the suppression of free fatty acid release by insulin and niacin is highly correlated (r = −0.93), indicating that individuals who are resistant to one are almost always resistant to the other.
In people with upper-body obesity or type 2 diabetes, fat cells cannot properly stop releasing fatty acids because the final control proteins that regulate fat breakdown are broken, no matter whether the signal comes from insulin or niacin.
What the research says
1 studyStudy: Adipose Tissue Resistance to the Antilipolytic Effect of Insulin and Niacin in Humans With Obesity.
In people with obesity or type 2 diabetes, if their fat cells don’t respond well to insulin telling them to stop releasing fat, they also don’t respond well to niacin doing the same thing — the two signals are equally weak in each person, even though they work differently at first.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.