Journal
JOURNAL OF FOOD AND DRUG ANALYSIS
Volume 24, Issue 4, Pages 754-761Publisher
FOOD & DRUG ADMINSTRATION
DOI: 10.1016/j.jfda.2016.03.005
Keywords
endoplasmic reticulum stress; fructose; insulin resistance; metabolic syndrome; oxidative stress
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Funding
- National Science Council, Taipei City, Taiwan, Republic of China [NSC 98-2313-B002-064]
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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. Copyright (C) 2016, Food and Drug Administration, Taiwan. Published by Elsevier Taiwan LLC.
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