Key result
Hyperinsulinemia from insulin receptor haploinsufficiency fails to alter atherosclerosis progression in ApoE-null mice.
Why the study?
Does hyperinsulinemia accelerate atherosclerosis development in Apolipoprotein E null mice?
Population
Female Apolipoprotein E null mice with knockout of a single allele of the insulin receptor gene and…
Comparison
Hyperinsulinemia induced by insulin receptor… vs Littermate controls with intact insulin receptors
Design
Preclinical
Follow-up
up to 52 weeks of age
Authors
Loading...
Hyperinsulinemia alone does not accelerate atherosclerosis in Apoe null mice; leaves open the role of insulin resistance or other factors in humans.
Does hyperinsulinemia accelerate atherosclerosis development in Apolipoprotein E null mice?
Absolute Event Rate: 14% vs 16.9%
p-value: p=0.6
Hyperinsulinemia alone, without substantial insulin resistance or changes in lipids/blood pressure, does not accelerate atherosclerosis in a mouse model.
Rask‐Madsen et al. (2012) studied Atherosclerosis susceptibility in hyperinsulinemia. Hyperinsulinemia (Insr haploinsufficiency) vs. Littermate controls with intact insulin receptors was evaluated on Atherosclerotic lesion size (en face lesion area in the aorta at 52 weeks) (p=0.6). Hyperinsulinemia due to insulin receptor haploinsufficiency did not significantly change atherosclerotic lesion size in Apoe null mice compared to controls.
Synapse has enriched 3 closely related papers on similar clinical questions. Consider them for comparative context: