Abstract
The peroxisome proliferator-activated receptor alpha (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 triacylglycerol (TG) and phospholipid (PL) as a result of starvation. In the present work, the effects of 72 h fasting on 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 than in WT mice fasted for the same length of time. Surprisingly, the total hepatic PL contents in fasted KO mice decreased by 45%, but no significant change in hepatic PL content was observed in WT mice following starvation. Gas chromatographic analysis indicated that KO mice were deprived of arachidonic (20:4n-6) and docosahexaenoic (22:6n-3) acids during fasting. Taken together, these results show that PPARalpha plays an important role in regulation of fatty acid metabolism as well as phospholipid homeostasis during energy deprivation.
Highlights
The peroxisome proliferator-activated receptor ␣ (PPAR␣) has been implicated as a key control of fatty acid catabolism during the cellular fasting
Was developed in fasted PPAR␣-null [knockout] (KO) mice Following 72 h of fasting, the body weight of WT mice was reduced by 24%
We show that PPAR␣ is a physiological regulator in maintaining the TG as well as PL homeostasis under energy deprivation
Summary
The peroxisome proliferator-activated receptor ␣ (PPAR␣) has been implicated as a key control of fatty acid catabolism during the cellular fasting. Definite proof that PPAR␣ plays a significant role in regulation of lipid homeostasis comes from the several starvation studies with PPAR␣-null (KO) mice [21,22,23,24,25,26] In these studies, short-term fasting (12–72 h) in KO mice resulted in hepatic steatosis, myocardial lipid accumulation, hypoketonemia, and hypoglycemia and it altered some gene expressions. Short-term fasting (12–72 h) in KO mice resulted in hepatic steatosis, myocardial lipid accumulation, hypoketonemia, and hypoglycemia and it altered some gene expressions Results of these studies clearly show that PPAR␣ plays a pivotal role in management of energy stores during fasting, a condition in which an increased requirement of hepatic fatty acid oxidation occurs
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