Requirement of PPARalpha in maintaining phospholipid and triglyceride homeostasis during energy deprivation

Susanna S. T. Lee, Wood-Yee Chan, Cherry K. C. Lo, David C. C. Wan, David S. C. Tsang, and Wing-Tai Cheung

Department of Biochemistry, Chinese University of Hong Kong, Hong Kong, Hong Kong

Corresponding Author: lee2022{at}cuhk.edu.hk

The PPARalpha has been implicated as a key control of fatty acid catabolism during the cellular fasting. However, little is known regarding changes of individual fatty acids in hepatic triglyceride (TG) and phospholipid (PL) as a result of starvation. In the present work, the effects of 72-h fasting on the hepatic TG and PL fatty acid profiles in PPARalpha-null (KO) mice and their wild-type (WT) counterparts were investigated. Our results indicated that mice deficient in PPARalpha displayed hepatomegaly and hypoketonemia following 72 h starvation. Histochemical analyses revealed that severe fatty infiltration was observed in the livers of KO mice under fasted conditions. Furthermore, 72-h fasting resulted in a 2.8-fold higher accumulation of hepatic TG in KO mice compared with the WT mice fasted for the same period of time. Surprisingly, the total hepatic PL contents in fasted KO mice decreased by 45%, while no significant changes in hepatic PL content was observed in WT mice following starvation. Gas chromatographic analysis indicated that PPARalpha-null mice were deprived of arachidonic (20:4n-6) and docosahexaenoic (22:6n-3) acids during fasting. Taken together, these results demonstrate that PPARalpha plays an important role in regulation of fatty acid metabolism as well as phospholipid homeostasis during energy deprivation.

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