Abstract
AimsTo compare the different serum peptidome patterns between twins with and without non-alcoholic fatty liver disease (NAFLD) in order to help understand the pathogenesis of NAFLD and to identify potential diagnostic and therapeutic targets.MethodsThe peptidomics patterns of 63 cases with NAFLD were compared with their twin healthy controls in Qingdao, China. Peptides between 800Da and 3500Da were captured and concentrated using C18 reversed-phase columns, followed by MALDI-TOF mass spectrometry. The sequences of peptides associated with NAFLD were further identified by MALDI-TOF-TOF. Further validation studies were conducted. One hundred additional serum samples were detected by commercially available ELISA kits to calculate the concentrations of complement C3f and fibrinopeptide A, respectively. The differences of these two peptides in the NAFLD and control groups were compared using SPSS 17.0, respectively.ResultsCompared with healthy controls, eleven peaks (861.1, 877.07, 904.5, 1206.57, 1350.64, 1518.7, 1690.9, 1777.94, 2931.29, 3190.4, 3261.4) were up-regulated and 7 peaks (942.44, 1020.47, 1060.06, 1211.7, 1263.63, 1449.76, 2768.3) were down-regulated in the NAFLD group. Two peptides derived from complement C3f and fibrinopeptide A, respectively, had the highest ROC values indistinguishing NAFLD cases from their normal controls. In the validation group, the concentrations of complement C3f and fibrinopeptide A (1466.929±78.306 pg/ml, 4.189±0.326 ng/ml, respevtively) in NAFLD group was higher than in control group (complement C3f 1159.357±99.624 pg/ml, FPA 3.039±0.483 ng/ml; P<0.05).ConclusionsIn this study, we established apeptidomics pattern that could help distinguish NAFLD patients from their twin controls. The differently-regulated peptides identified in our study may be potential diagnostic markers or therapeutic targets for NAFLD.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is a cause of chronic liver disease that has gained increasing recognition over the past decade
The condition most commonly associated with NAFLD is chronic over nutrition with consequent obesity [1,2,3] and, often, insulin resistance [4,5]
The biological basis for the wide histological spectrum that occurs in NAFLD remains poorly defined
Summary
Nonalcoholic fatty liver disease (NAFLD) is a cause of chronic liver disease that has gained increasing recognition over the past decade. New genomic and proteomic technologies have the potential to understand the complex pathogenic mechanisms of NAFLD [10,11,12,13,14,15]. Simultaneous assessment of gene expression in a large number of genes and protein peaks can help identify molecular pathways that are active in NAFLD [11,12,13,14,15,16]. Proteomic analyses have been limited by poor sensitivity in detecting lowabundance proteins as well as difficulties with maintaining sample stability and data management. Recent advances in protein separation and improvements in both detection and identification of peptides and proteins have facilitated detailed characterization of complex biological samples, including the liver domain.
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