Key result
Cold exposure down-regulates ANGPTL4 in brown adipose tissue to enhance LPL activity and fatty acid uptake, while up-regulating it in white adipose tissue to direct plasma triglycerides to BAT.
Population
Preclinical model (brown and white adipose tissue)
Design
Preclinical
Authors
Loading...
ANGPTL4 regulates cold-induced triglyceride partitioning to BAT in mice; hypothesis-generating for human cardiometabolic therapies, requires validation.
ANGPTL4 is a critical mechanistic regulator that directs plasma lipid partitioning to brown adipose tissue during sustained cold exposure.
Dijk et al. (2015) studied this question. Cold exposure and Angptl4 genetic manipulation vs. Thermoneutrality (28°C) and wild-type mice was evaluated on LPL activity and TRL-derived fatty acid uptake in brown and white adipose tissue. Cold exposure down-regulates ANGPTL4 in brown adipose tissue to enhance LPL activity and fatty acid uptake, while up-regulating it in white adipose tissue to direct plasma triglycerides to BAT.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: