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Sodium Butyrate-Modulated Mitochondrial Function in High-Insulin Induced HepG2 Cell Dysfunction
Zhao,Tingting1; Gu,Junling1; Zhang,Huixia1; Wang,Zhe1; Zhang,Wenqian1; Zhao,Yonghua2; Zheng,Ying2; Zhang,Wei1; Zhou,Hua1,3; Zhang,Guilin1; Sun,Qingmin4; Zhou,Enchao4; Liu,Zhilong3; Xu,Youhua1,3
Source PublicationOxidative Medicine and Cellular Longevity

The liver plays a pivotal role in maintaining euglycemia. Biogenesis and function of mitochondria within hepatocytes are often the first to be damaged in a diabetic population, and restoring its function is recently believed to be a promising strategy on inhibiting the progression of diabetes. Previously, we demonstrated that the gut microbiota metabolite butyrate could reduce hyperglycemia and modulate the metabolism of glycogen in both db/db mice and HepG2 cells. To further explore the mechanism of butyrate in controlling energy metabolism, we investigated its influence and underlying mechanism on the biogenesis and function of mitochondria within high insulin-induced hepatocytes in this study. We found that butyrate significantly modulated the expression of 54 genes participating in mitochondrial energy metabolism by a PCR array kit, both the content of mitochondrial DNA and production of ATP were enhanced, expressions of histone deacetylases 3 and 4 were inhibited, beta-oxidation of fatty acids was increased, and oxidative stress damage was ameliorated at the same time. A mechanism study showed that expression of GPR43 and its downstream protein beta-arrestin2 was increased on butyrate administration and that activation of Akt was inhibited, while the AMPK-PGC-1alpha signaling pathway and expression of p-GSK3 were enhanced. In conclusion, we found in the present study that butyrate could significantly promote biogenesis and function of mitochondria under high insulin circumstances, and the GPR43-β-arrestin2-AMPK-PGC1-alpha signaling pathway contributed to these effects. Our present findings will bring new insight on the pivotal role of metabolites from microbiota on maintaining euglycemia in diabetic population.

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Indexed BySCIE
WOS Research AreaCell Biology
WOS SubjectCell Biology
WOS IDWOS:000556574600003
Scopus ID2-s2.0-85088879807
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Cited Times [WOS]:10   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionUniversity of Macau
Corresponding AuthorXu,Youhua
Affiliation1.Faculty of Chinese Medicine,State Key Laboratory of Quality Research in Chinese Medicine,Macau University of Science and Technology,Taipa, Macao,Macao
2.Institute of Chinese Medical Sciences,State Key Laboratory of Quality Research in Chinese Medicine,University of Macau,Taipa, Macao,Macao
3.Department of Endocrinology,Zhuhai Hospital of Integrated Traditional Chinese and Western Medicine,Zhuhai,China
4.Jiangsu Province Hospital of Traditional Chinese Medicine,Affiliated Hospital of Nanjing University of Chinese Medicine,Nanjing,Hanzhong Road,China
First Author AffilicationUniversity of Macau
Corresponding Author AffilicationUniversity of Macau
Recommended Citation
GB/T 7714
Zhao,Tingting,Gu,Junling,Zhang,Huixia,et al. Sodium Butyrate-Modulated Mitochondrial Function in High-Insulin Induced HepG2 Cell Dysfunction[J]. Oxidative Medicine and Cellular Longevity,2020,2020.
APA Zhao,Tingting,Gu,Junling,Zhang,Huixia,Wang,Zhe,Zhang,Wenqian,Zhao,Yonghua,Zheng,Ying,Zhang,Wei,Zhou,Hua,Zhang,Guilin,Sun,Qingmin,Zhou,Enchao,Liu,Zhilong,&Xu,Youhua.(2020).Sodium Butyrate-Modulated Mitochondrial Function in High-Insulin Induced HepG2 Cell Dysfunction.Oxidative Medicine and Cellular Longevity,2020.
MLA Zhao,Tingting,et al."Sodium Butyrate-Modulated Mitochondrial Function in High-Insulin Induced HepG2 Cell Dysfunction".Oxidative Medicine and Cellular Longevity 2020(2020).
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