Key result
ApoA-I deficiency in mice significantly inhibited the loss of body fat during caloric restriction (27.6% vs 39.9% in wild-type) by blunting stimulated adipose tissue lipolysis.
Why the study?
Does apoA-I level modulate body weight and adipose tissue lipolysis in mice fed an obesogenic diet?
Population
Male C57BL/6 wild-type, apoA-I deficient (apoA-I) and apoA-I transgenic (apoA-I) mice fed obesogenic diets…
Comparison
ApoA-I deficiency (apoA-I) or ApoA-I… vs Wild-type (WT) mice
Design
Preclinical
Follow-up
20 weeks
Authors
Loading...
Should not yet inform clinical practice; leaves open apoA-I as a modulator of lipolysis for obesity research.
Does apoA-I level modulate body weight and adipose tissue lipolysis in mice fed an obesogenic diet?
Absolute Event Rate: 27.6% vs 39.9%
p-value: p=<0.05
ApoA-I and HDL modulate body fat content by controlling the extent of lipolysis, suggesting they are key components of lipid metabolism in adipose tissue and potential therapeutic targets in obesity.
Averill et al. (2014) studied Obesity (n=56). ApoA-I deficiency vs. Wild-type mice was evaluated on Relative loss of body fat during caloric restriction (p=<0.05). ApoA-I deficiency in mice significantly inhibited the loss of body fat during caloric restriction (27.6% vs 39.9% in wild-type) by blunting stimulated adipose tissue lipolysis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: