The first study on the effect of crocodile oil from Crocodylus siamensis on hepatic mitochondrial function for energy homeostasis in rats
Issued Date
2022-04-01
Resource Type
ISSN
09728988
eISSN
22310916
Scopus ID
2-s2.0-85129578472
Journal Title
Veterinary World
Volume
15
Issue
4
Start Page
986
End Page
997
Rights Holder(s)
SCOPUS
Bibliographic Citation
Veterinary World Vol.15 No.4 (2022) , 986-997
Suggested Citation
Parunyakul K., Srisuksai K., Santativongchai P., Pongchairerk U., Ampawong S., Tulayakul P., Fungfuang W. The first study on the effect of crocodile oil from Crocodylus siamensis on hepatic mitochondrial function for energy homeostasis in rats. Veterinary World Vol.15 No.4 (2022) , 986-997. 997. doi:10.14202/vetworld.2022.986-997 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/87084
Title
The first study on the effect of crocodile oil from Crocodylus siamensis on hepatic mitochondrial function for energy homeostasis in rats
Other Contributor(s)
Abstract
Background and Aim: Consumption of fatty acids (FA) can alter hepatic energy metabolism and mitochondrial function in the liver. Crocodile oil (CO) is rich in mono-and polyunsaturated FAs, which have natural anti-inflammatory and healing properties. In rat livers, we investigated the effect of CO on mitochondrial function for energy homeostasis. Materials and Methods: Twenty-one male Sprague-Dawley rats were divided into three groups at random. Group 1 rats were given sterile water (RO), Group 2 rats were given CO (3% v/w), and Group 3 rats were given palm oil (PO) (3% v/w). For 7 weeks, rats were given sterile water, CO, and PO orally. The researchers looked at body weight, food intake, liver weight, energy intake, blood lipid profiles, and mitochondria-targeted metabolites in the liver. The liver’s histopathology, mitochondrial architecture, and hydrolase domain containing 3 (HDHD3) protein expression in liver mitochondria were studied. Results: Body weight, liver weight, liver index, dietary energy intake, and serum lipid profiles were all unaffected by CO treatment. The CO group consumed significantly less food than the RO group. The CO group also had significantly higher levels of oxaloacetate and malate than the PO group. CO treatment significantly ameliorated hepatic steatosis, as evidenced by a greater decrease in the total surface area of lipid particles than PO treatment. CO administration preserved mitochondrial morphology in the liver by upregulating the energetic maintenance protein HDHD3. Furthermore, chemical-protein interactions revealed that HDHD3 was linked to the energy homeostatic pathway. Conclusion: CO may benefit liver function by preserving hepatic mitochondrial architecture and increasing energy metabolic activity.