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Abstract Title:

Phloretin attenuation of hepatic steatosisan improvement of mitochondrial dysfunction by activating AMPK-dependent signaling pathways in C57BL/6J mice and HepG2 cells.

Abstract Source:

Food Funct. 2021 Dec 13 ;12(24):12421-12433. Epub 2021 Dec 13. PMID: 34788781

Abstract Author(s):

Lin Han, Yao Zhang, Jia Li, Yao Xiao, Mei Lu, Yunlong Li, Min Wang

Article Affiliation:

Lin Han

Abstract:

Phloretin, a dihydrochalcone, widely exists in the fruits of apple trees and crabapple trees () with multiple biological activities. Presently, we studied the function of phloretin on the attenuation of hepatic steatosis and further explored the underlying mechanisms bothand. Male C57BL/6J mice were fed a normal diet or high fat diet (HFD) with or without phloretin (100 mg kg) for 12 weeks. HepG2 cells were induced by 200μM palmitic acid (PA) and co-incubated with phloretin (50 μM) for 24 h. The results showed that phloretin treatment significantly decreased the accumulation of lipids in the liver of the HFD-fed C57BL/6J mice and PA-induced HepG2 cells. Also, phloretin effectively ameliorated hepatic steatosispromoting fatty acidβ-oxidation (FAO). This biological activity of phloretin was closely related to its capacity to improve mitochondrial dysfunction, including the promotion of mitochondrial biosynthesis and inhibition of mitochondrial swelling through the AMPK-dependent SIRT1/PGC-1α and SIRT3/CypD signaling pathways, respectively. These results demonstrate that phloretin effectively improves mitochondrial function and ameliorates HFD-induced hepatic steatosis through an AMPK-dependent signaling pathway.

Study Type : Animal Study, In Vitro Study

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