Sodium Butyrate-Modulated Mitochondrial Function in High-Insulin Induced HepG2 Cell Dysfunction

المؤلفون المشاركون

Zhou, Hua
Xu, Youhua
Zhang, Wei
Zhao, Tingting
Gu, Junling
Zhang, Huixia
Wang, Zhe
Zhang, Wenqian
Zhao, Yonghua
Zheng, Ying
Zhang, Guilin
Sun, Qingmin
Zhou, Enchao
Liu, Zhilong

المصدر

Oxidative Medicine and Cellular Longevity

العدد

المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-16، 16ص.

الناشر

Hindawi Publishing Corporation

تاريخ النشر

2020-07-17

دولة النشر

مصر

عدد الصفحات

16

التخصصات الرئيسية

الأحياء

الملخص EN

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.

نمط استشهاد جمعية علماء النفس الأمريكية (APA)

Zhao, Tingting& Gu, Junling& Zhang, Huixia& Wang, Zhe& Zhang, Wenqian& Zhao, Yonghua…[et al.]. 2020. Sodium Butyrate-Modulated Mitochondrial Function in High-Insulin Induced HepG2 Cell Dysfunction. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-16.
https://search.emarefa.net/detail/BIM-1203850

نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)

Zhao, Tingting…[et al.]. Sodium Butyrate-Modulated Mitochondrial Function in High-Insulin Induced HepG2 Cell Dysfunction. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-16.
https://search.emarefa.net/detail/BIM-1203850

نمط استشهاد الجمعية الطبية الأمريكية (AMA)

Zhao, Tingting& Gu, Junling& Zhang, Huixia& Wang, Zhe& Zhang, Wenqian& Zhao, Yonghua…[et al.]. Sodium Butyrate-Modulated Mitochondrial Function in High-Insulin Induced HepG2 Cell Dysfunction. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-16.
https://search.emarefa.net/detail/BIM-1203850

نوع البيانات

مقالات

لغة النص

الإنجليزية

الملاحظات

Includes bibliographical references

رقم السجل

BIM-1203850