Effects of Constant Light Exposure on Hepatic Lipid Metabolism and Weight Gain
ZHU Kuicheng1, DU Chunyan1, HE Long2*
The exposure to ALAN (articial light at night) disrupts the biological rhythms and has been associated with metabolic disorders, but the underlying mechanism is not known. A random allocation of male 8-week C57BL/6 mice into three groups was done, including controls, light group and fenofibrate groups, which contained 20 mice each. The body weight, liver wet weight of the mice were measured. Liver index was calculated based on the percentage of liver to body weight while pathological changes of the liver and fat tissue were observed microscopically. The contents of TG (triglyceride) were analysed in both serum and liver by enzymatic assays, while oil red O staining in liver frozen sections were performed to confirm hepatic lipid cumulation. The hypothalamus and liver were collected for mechanism experimentation using RT-qPCR. Fenofibrate (agonist of PPARα) was used to confirm the relationship between PPARα and lipidolysis. The results showed that the mice exposed to ALAN developed obesity and hepatic steatosis. Biochemical analysis suggested increased hepatic lipid accumulated and increased transport of lipid from the liver to adipose tissues in LL mice that gained weight under constant light exposure. The expression of key genes involved in fatty acid oxidation (Pgc1α, Pparα, Cpt1a and Aco, etc) was
significantly increased, which was paralleled by decreased expression of Rev-erbα. Additionally, a decrease in adipose tissue weight and adipocyte size led to the differences in body weights when treated with fenofibrate, which reversed hepatic lipid deposition by promoting the expression of lipid decomposition gene Pparα. As a reminder, constant light disrupts the body clock, thus leading to obesity. The biological process may be related to inhibiting the expression of FAO (fatty acid oxidation) genes.
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