ArticleJournal of traditional Chinese medicine = Chung i tsa chih ying wen pan2023
Mitochondrial dysfunction in a rat model and the related risk of metabolic disorders.
Article in Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- The complete mitochondrial genome of Prinsepia uniflora (Rosaceae): De novo assembly, characterization, and phylogenetic analysis.BMC genomics · 2026Article
- High fat diet exacerbated glycolipid metabolism disorder in kidney Yang deficiency rats by interfering with IRS 1-PI3K (p85) -Akt-GLUT 4 pathway.Lipids in health and disease · 2025Article
- Wenyang-Tianjing-Jieyu Decoction Improves Depression Rats of Kidney Yang Deficiency Pattern by Regulating T Cell Homeostasis and Inflammation Level.Neuropsychiatric disease and treatment · 2024Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
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Abstract
objectiveTo explore whether kidney deficiency (KYD) is prone to metabolic disorders may be linked to impaired mitochondrial function in thermogenesis and metabolic tissues.
methodsA rat model of KYD was used, which was established using Sprague Dawley rat dams with warm preference subjected to herbal treatment that can improve kidney . The human relevance was confirmed by reduced serum corticosterone levels, and increased preference for warm location.
resultsKYD Rats were underdeveloped. Adenosine-triphosphate (ATP) production was reduced in the brown fat, but increased in the muscle. However, oxidative phosphorylated complexes to generate ATP and mitochondrial biogenesis marker were reduced in both tissues. When the second insult of high-fat diet (HFD) was introduced, KYD rats gained less weight yet developed more severe lipid and glucose metabolic disorders. This may be driven by disregulated liver gluconeogenesis marker forkhead box protein O1 and lipid metabolic regulator cholesterol 7 alpha-hydroxylase.
conclusionKYD rats exhibited reduced mito-chondrial function in the brown fat, but were partially compensated by skeletal muscle, associated with the phenotype of warm preference and metabolic disorder, which was further exacerbated by additional HFD consumption. Future studies can focus on treatment targetting mitochondria function to reverse this phenotype.
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