Proteomic changes associated with metabolic syndrome in a fructose-fed rat model
Cheng-Chu Hsieh a,b,1, Chen-Chung Liao c,1, Yi-Chun Liao d,1,
Lucy Sun Hwang e, Liang-Yi Wu f, Shu-Chen Hsieh e,*
a Department and Institute of Veterinary Medicine, School of Veterinary Medicine, National Taiwan University,
Taipei, Taiwan
b Biologics Division, Animal Health Research Institute, Council of Agriculture, Executive Yuan, New Taipei, Taiwan
c Proteomics Research Center, National Yang-Ming University, Taipei, Taiwan
d Department of Biochemical Science and Technology, National Taiwan University, Taipei, Taiwan
e Institute of Food Science and Technology, National Taiwan University, Taipei, Taiwan
f Department of Bioscience Technology, Chung Yuan Christian University, Taoyuan City, Taiwan
Metabolic syndrome (MetS), characterized by a constellation of disorders such as hyperglycemia, insulin resistance, and hypertension, is becoming a major global public health problem. Fructose consumption has increased dramatically over the past several decades and with it the incidence of MetS. However, its molecular mechanisms remain to be explored. In this study, we used male Sprague-Dawley (SD) rats to study the pathological mechanism of fructose induced MetS. The SD rats were fed a 60% high-fructose diet for 16 weeks to induce MetS. The induction of MetS was confirmed by blood biochemistry examination. Proteomics were used to investigate the differential hepatic protein expression patterns between the normal group and the MetS group. Proteomic results revealed that fructose-induced MetS induced changes in glucose and fatty acid metabolic pathways. In addition, oxidative stress and endoplasmic reticulum stress-related proteins were modulated by high-fructose feeding. In summary, our results identify many new targets for future investigation. Further characterization of these proteins and their involvement in the link between insulin resistance and metabolic dyslipidemia may bring new insights into MetS.
Keywords: endoplasmic reticulum stress, fructose, insulin resistance, metabolic syndrome, oxidative stress