Journal
ELECTROPHORESIS
Volume 36, Issue 17, Pages 2002-2016Publisher
WILEY
DOI: 10.1002/elps.201500076
Keywords
Ameliorative mechanism; Comparative proteomics; Fat accumulation; Fuzhuan brick tea extract (FTE); Nonalcoholic fatty liver disease
Funding
- National Natural Science Foundation of China [31100502]
- Scientific Research Fund of Hunan Provincial Education Department [12B064]
- Specialized Research Foundation for the doctorial Program of Higher Education of China [20114320120004]
- Key Project of National Technology Innovation System for Tea Industry in the People's Republic of China [CARS-23]
- Foundation for Innovation Research Team of Ministry of Education [IRT0963]
- Hunan Provincial Natural Science Foundation of China [13JJ4067]
- 1515 Talents Project of Hunan Agricultural University
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Fuzhuan brick tea has received increasing attention in recent years owing to its benefits for nonalcoholic fatty liver disease (NAFLD) and associated metabolic syndrome. For exploring the ameliorative mechanism, the liver proteomes from three groups of rats fed either a normal control diet (NCD), a high fat diet (HFD), or a HFD supplemented with high-dose Fuzhuan brick tea extract (FTE) (HFD + HFTE) were comprehensively compared by quantitative proteomics using 2DE-LC-MS/MS. This is the first study of the effects of tea aqueous extract on the liver proteome of rats suffering from metabolic syndrome. The results showed that 57 proteins displayed more than 1.5-fold differences in at least one of two comparisons of HFD versus NCD and HFD versus HFD + HFTE due to HFD feeding and FTE treatment, respectively. Of them, over 75% of proteins exhibited a similar tendency of expression in the two comparisons, meaning FTE was able to correct HFD effects on rat livers. By function analyses, an extensive list of proteins was involved in sugar and lipid metabolism. Compared with HFD-fed rats, the reduced lipogenesis and enhanced -oxidation, tricarboxylic acid cycle and respiratory chain in HFD + HFTE-fed rats, which mainly contributed to ameliorate hepatic fat accumulation and associated NAFLD. Additionally, some putative drug targets were also revealed such as COX2, PGAM1, ACACB, FAS, and ECHS1.
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