Living organisms store excess energy as fat to survive and reproduce. However, excessive energy storage will cause obesity and increase the risk of metabolic diseases, such as type 2 diabetes and heart disease. White adipose tissue (WAT) and brown adipose tissue (BAT) represent energy storage and energy expenditure organs, respectively. Beige (or brite) adipocytes are a new class of adipocytes widely distributed in WAT. Beige adipocytes can be induced to become browning adipocytes at low temperature. This feature has attracted broad interest as a potential way to increase energy expenditure and protect against obesity.
Triglycerides (TGs) in the blood supply peripheral tissues with metabolic fuel, but they can only be absorbed and utilized as free fatty acids after being hydrolyzed by lipoprotein lipase (LPL), a TG hydrolase located in the capillary endothelium of all peripheral tissues. Previous studies have shown that feeding can increase LPL activity in WAT, thereby facilitating TG uptake and storage. Meanwhile, feeding inhibits LPL activity in energy-consuming organs like the heart, muscles, and brown adipose tissue. Fasting can reverse these processes. A fascinating question is whether and how feeding regulates LPL activity and TG uptake in BAT in response to physiological changes.
To answer this question, Yan Wang lab at Wuhan University recently published their findings in Life Metabolism, which titled "Chronic cold exposure reprograms feeding-regulated LPL activity in white adipose tissues through hepatic ANGPTL3 and ANGPTL8". They found that prolonged cold exposure reverses feeding-regulated LPL activity during browning in WAT. They further revealed that the hepatic insulin signaling pathway, as well as hepatic secretion factors ANGPTL3 and ANGPTL8, plays a crucial role in this process (Figure 1).
