Overexpressing a protein involved in the uptake of fat in muscle of mice can improve their tolerance to cold temperatures, researchers find in a new study that showcases the over-looked role muscle may play in the cold response.
When temperatures drop, mammals respond by generating heat (thermogenesis), through mechanisms like shivering and breaking down ‘brown fat’ (high energy fat cells that are especially prominent in newborns and hibernating animals).
Considering that muscle accounts for over one-third of body mass and muscle activity regulates fat metabolism, Dalan Jensen and colleagues found that increasing the muscle’s ability to use fat for energy had a profound impact on its contribution to thermogenesis.
They generated mice overexpressing lipoprotein lipase (LPL), an enzyme that extracts fat from the blood so that it can be used to produce energy instead of sugar. They placed LPL mice in a chamber set to 4 °C (39 °F) and found that they were far more cold tolerant than regular mice; LPL mice could withstand 4 °C for several hours and still maintain normal body temperatures.
This tolerance came from LPL’s ability to increase the muscle’s ability to oxidize fat, which allow LPL mice to produce more heat than regular animals without increasing their physical activity. Interestingly, this enhanced muscular thermogenesis is akin to how birds –which lack brown fat—produce heat and suggests that mammals, too, have multiple avenues to try and stay warm.
Article: Lorraine Shelly, Lori Royer, Thomas Sand, Heather Jensen, and Yi Luo, Phospholipid transfer protein deficiency ameliorates diet-induced hypercholesterolemia and inflammation in mice, J. Lipid Res. 2008 49: 773-781. First Published on January 14, 2008; doi:10.1194/jlr.M700336-JLR200
