Abstract
BackgroundsMitochondria plays a critical role in the development and pathogenesis of nonalcoholic fatty liver disease (NAFLD). Neohesperidin (NHP) could lower blood glucose and prevent obesity in mice. However, the direct effect of NHP on hepatic steatosis has not been reported.MethodsMice were fed with either a chow diet or HFD with or without oral gavage of NHP for 12 weeks. A variety of biochemical and histological indicators were examined. In vitro cell culture model was utilized to demonstrate underlying molecular mechanism of the effect induced by NHP treatment.ResultsNHP increases mitochondrial biogenesis, improves hepatic steatosis and systematic insulin resistance in high fat diet (HFD) fed mice. NHP elevates hepatic mitochondrial biogenesis and fatty acid oxidation by increasing PGC-1α expression. Mechanistically, the activation of AMP-activated protein kinase (AMPK) is involved in NHP induced PGC-1α expression.ConclusionsPGC-1α-mediated mitochondrial biogenesis plays a vital role in the mitigation of hepatic steatosis treated by NHP. Our result suggests that NHP is a good candidate to be dietary supplement for the auxiliary treatment of NAFLD.
Highlights
Hypercaloric diet is one of the main factors leading to metabolic syndrome, mainly manifested as obesity, hyperlipidemia, insulin resistance and fatty liver, among others[1]
We found that NHP elevated PGC-1α expression and hepatic mitochondrial biogenesis in high fat diet (HFD) fed mice
Administration of NHP obviously relieved hepatic steatosis in HFD mice indicated by hematoxylin and eosin (H&E) staining (Fig. 1c) and Nonalcoholic fatty liver disease (NAFLD) activity score (NAS) evaluation (Fig. 1d)
Summary
Hypercaloric diet is one of the main factors leading to metabolic syndrome, mainly manifested as obesity, hyperlipidemia, insulin resistance and fatty liver, among others[1]. Nonalcoholic fatty liver disease (NAFLD), which is characterized by the accumulation of excess fat in the liver of people who drink little or no alcohol[2], is increasingly recognized as the hepatic manifestation of metabolic syndrome. Previous researches have shown a 40% decrease in hepatic PGC-1α expression in NAFLD patients, accompanied by mitochondrial dysfunction, lipid accumulation, and insulin resistance[9,10]. The treatment that stimulates mitochondrial function can delay the progression of obesity and diabetes[5].
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