ArticleBiomolecules2022
Crocodile Oil Disrupts Mitochondrial Homeostasis and Exacerbates Diabetic Kidney Injury in Spontaneously Diabetic Torii Rats.
Article in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- An integrative bioinformatic and Mendelian randomization study exploring the role of polyunsaturated fatty acid metabolism in laryngeal cancer.Discover oncology · 2025Article
- Recent advances in crocodilian oil research: bioactive components and potential therapeutic applications.Frontiers in medicine · 2025Review
- Dietary factors and risk for adverse pregnancy outcome: A Mendelian randomization analysis.Food science & nutrition · 2024Article
- Redox Imbalance and Mitochondrial Abnormalities in Kidney Disease-Volume II.Biomolecules · 2024Article
- Antioxidant Activity of Crocodile Oil (Foods (Basel, Switzerland) · 2023Article
- New therapeutic directions in type II diabetes and its complications: mitochondrial dynamics.Frontiers in endocrinology · 2023Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
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Abstract
Diabetic nephropathy is currently the leading cause of end-stage renal disease (ESRD) in type 2 diabetes. Studies have suggested that supplementation with some fatty acids might reduce the risk and delay the progression to ESRD in patient with chronic kidney disease. Crocodile oil (CO) contains a variety of fatty acids, especially omega-3, -6 and -9, that have been reported to be beneficial to human health. This study examined the impact of long-term CO supplementation on the development of diabetic nephropathy in spontaneously diabetic Torii (SDT) rats. After diabetic verification, SDT rats were assigned to receive vehicle or CO at 500 and 1000 mg/kg BW, respectively, by oral gavage. Age-matched nondiabetic Sprague-Dawley rats were given vehicle or high-dose CO. After 28 weeks of intervention, CO failed to improve hyperglycemia and pancreatic histopathological changes in SDT rats. Unexpectedly, CO dose-dependently exacerbated the impairment of kidney and mitochondrial functions caused by diabetes. CO also disturbed the expressions of proteins involved in mitochondrial biogenesis, dynamics, and mitophagy. However, no significant alterations were observed in nondiabetic rats receiving high-dose CO. The findings reveal that CO has deleterious effects that aggravate diabetic kidney injury via disrupting mitochondrial homeostasis, possibly due to its improper omega-6: omega-3 ratio.
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