期刊
EXPERIMENTAL AND THERAPEUTIC MEDICINE
卷 2, 期 2, 页码 309-315出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2011.208
关键词
diet-induced obesity; high-fat diet; enoyl coenzyme A hydratase 1; peroxisomal; peroxisome proliferator-activated receptor alpha
资金
- National Natural Science Foundation of China [30871428, 81072680]
- Natural Science Foundation of Guangdong Province [10151805702000002]
- Specialized Research Fund for the Doctoral Program of Higher Education of China [20100002120017]
- China Postdoctoral Science Foundation [20060390460]
- Tertiary College Science Foundation of Nanshan, Shenzhen [2008028]
This study aimed to investigate the potential mechanisms of natural resistance to high-fat diet-induced obesity. Four-week-old C57BL/6 mice were fed a high-fat diet for 6 weeks and were then designated as high-fat diet-fed obesity-prone (HOP) and obesity-resistant (HOR) animals. Their blood biochemistry was evaluated, and visceral adipose tissue samples were subjected to proteomic, Western blot and quantitative real-time PCR (q-PCR) analyses. The HOR mice showed reduced visceral fat weight and size, as well as lowered serum lipid and leptin levels. Proteomic analysis showed that enoyl coenzyme A hydratase 1, peroxisomal (Ech1) expression was significantly increased in their visceral adipose tissues. Moreover, other proteins, such as alpha-tropomyosin, myosin light chain, urine-nucleoside phosphorylase and transgelin, were also significantly increased. Furthermore, q-PCR analysis showed that the expression of acyl-CoA oxidase 1 palmitoyl, enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase and 3-oxoacyl-CoA thiolase responsible for peroxisomal beta-oxidation was also up-regulated in the visceral adipose tissues of the HOR mice. The expression of peroxisome proliferator-activated receptor alpha (PPAR alpha) was increased in the HOR mice as shown by Western blot analysis. Obesity-resistant animals show enhanced peroxisomal beta-oxidation metabolism and reduced fat accumulation in visceral adipose tissues by up-regulating the expression of Echl, peroxisomal or other related peroxisomal beta-oxidation marker genes, which may be driven or enhanced by the up-regulation of the expression of PPAR alpha. However, further validation in future studies is required.
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