Syarifah Dewi - Department of Biochemistry and Molecular Biology, Faculty of Medicine Universitas Indonesia, Jakarta, Indonesia & Center of Hypoxia and Oxidative Stress Studies, Faculty of Medicine Universitas Indonesia, Jakarta, Indonesia.
Yulhasri Yulhasri - Department of Biochemistry and Molecular Biology, Faculty of Medicine Universitas Indonesia, Jakarta, Indonesia & Center of Hypoxia and Oxidative Stress Studies, Faculty of Medicine Universitas Indonesia, Jakarta, Indonesia.
Wawan Mulyawan - Department of Aerophysiology, Lakespra Saryanto, Air Force Indonesian National Army, Jakarta, Indonesia.

Background: In a hypoxic state, fatty acid breakdown reaction may be inhibited due to a lack of oxygen. It is likely that the fatty acids will be stored as triacylglycerol. The aim of this study was to analyse triacylglycerol synthesis in the liver after intermittent hypobaric hypoxia (HH) exposures. Methods: Samples are liver tissues from ۲۵ male Wistar rats were divided into ۵ groups: control group (normoxia), group I (once HH exposure), group II (twice HH exposures), group III (three-times HH exposures) and group IV (four-times HH exposures). The triacylglycerol level, mRNA expression of HIF-۱α and PPAR-γ were measured in rat liver from each group. Results: We demonstrated that triacylglycerol level, mRNA expression of HIF-۱α and PPAR-γ is elevated in group I significantly compared to control group. In the intermittent HH groups (group II, III and IV), mRNA expression of HIF-۱α and PPAR-γ tends to downregulate near to control group. However, the triacylglycerol level is still found increased in the intermittent HH exposures groups. Significant increasing of triacylglycerol level was found especially in group IV compared to control group.  Conclusions: We conclude that intermittent HH exposures will increase the triacylglycerol level in rat liver, supported by the increasing of HIF-۱α and PPAR-γ mRNA expression that act as  transcription factor to promote triacylglycerol synthesis.

Hypoxia, Triacylglycerol, Liver, HIF-۱α, PPAR-γ