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Chen S.,Hebei Research Institute for Endocrine and Metabolic Diseases | Sun L.,Hebei Medical University | Gao H.,Hebei Medical University | Ren L.,Hebei Research Institute for Endocrine and Metabolic Diseases | And 2 more authors.
Endocrine Research | Year: 2015

Purpose/Aims of the study: This study sought to study the levels of circulating endothelial progenitor cells (EPCs), serum visfatin, and oxidative stress in obese individuals, and their respective correlations. Materials and methods: The circulating levels of EPCs were measured through detecting CD309 and CD34 by flow cytometry. Serum visfatin concentration was measured by enzyme-linked immunosorbent assay in 31 obese men [obese group: BMI 28.9±0.86kg/m2; age 44.93±1.78 years (range 40 to 47)] and 30 normal-weight men [control group: BMI 22.7±1.22kg/m2; age 44.03±1.87 years (range 41 to 47)]. Indexes of oxidative stress were assayed by a colorimetric method. The relationships between circulating EPCs, serum visfatin, and oxidative stress markers were further analyzed by multiple linear regression analysis. Statistical significance was set at p<0.05. Results: The obese group showed higher levels of serum visfatin and a lower level of circulating EPCs compared with controls. Serum superoxide dismutase (SOD) activity, total antioxidant capacity (T-AOC), and glutathione peroxidase (GSH-px) activity were significantly lower in obese subjects than in controls, while levels of serum malondialdehyde (MDA) were significantly higher. Circulating EPCs were positively associated with SOD (β=0.306) and LnHOMA-IR (β=0.223) and negatively associated with BMI (β=-0.321), serum visfatin (β=-0.236), and MDA (β=-0.293). Conclusions: The quantity of circulating EPCs decreases in obese individuals, along with increased serum visfatin and oxidative stress product. Visfatin and oxidative stress might therefore impact on the circulating EPCs in obese populations. © 2015 Informa Healthcare USA, Inc. Source

Song G.-Y.,General Hospital of Hebei | Song G.-Y.,Hebei Research Institute for Endocrine and Metabolic Diseases | Ren L.-P.,General Hospital of Hebei | Ren L.-P.,Hebei Research Institute for Endocrine and Metabolic Diseases | And 12 more authors.
Clinical and Experimental Pharmacology and Physiology | Year: 2012

The aim of the present study was to investigate the effects of high fructose and high fat feeding on muscle lipid metabolism and to illustrate the mechanisms by which the two different dietary factors induce muscle lipid accumulation. C57BL/J6 mice were fed either a standard, high-fructose (HFru) or high-fat diet. After 16 weeks feeding, mice were killed and plasma triglyceride (TG) and free fatty acid (FFA) levels were detected. In addition, muscle TG and long chain acyl CoA (LCACoA) content was determined, glucose tolerance was evaluated and the protein content of fatty acid translocase CD36 (FATCD36) in muscle was measured. Mitochondrial oxidative function in the muscle was evaluated by estimating the activity of oxidative enzymes, namely cytochrome oxidase (COx), citrate synthase (CS) and β-hydroxyacyl CoA dehydrogenase (β-HAD), and the muscle protein content of carnitine palmitoyltransferase-1 (CPT-1), cyclo-oxygenase (COX)-1 and proliferator-activated receptor coactivator (PGC)-1α was determined. Finally, sterol regulatory element-binding protein-1c (SREBP-1c) gene expression and fatty acid synthase (FAS) protein content were determined in muscle tissues. After 16 weeks, plasma TG and FFA levels were significantly increased in both the HFru and HF groups. In addition, mice in both groups exhibited significant increases in muscle TG and LCACoA content. Compared with mice fed the standard diet (control group), those in the HFru and HF groups developed glucose intolerance and exhibited increased FATCD36 protein levels, enzyme activity related to fatty acid utilization in the mitochondria and protein expressions of CPT-1, COX-1 and PGC-1α in muscle tissue. Finally, mice in both the HFru and HF groups exhibited increase SREBP-1c expression and FAS protein content. In conclusion, high fructose and high fat feeding lead to similar changes in muscle lipid metabolism in C57BL/J6 mice. Lipid accumulation in the muscle may be associated with increased expression of proteins related to lipid transportation and synthesis. © 2012 The Authors. Clinical and Experimental Pharmacology and Physiology © 2012 Wiley Publishing Asia Pty Ltd. Source

Sun Y.,Hebei General Hospital | Sun Y.,Hebei Research Institute for Endocrine and Metabolic Diseases | Chen S.,Hebei General Hospital | Chen S.,Hebei Research Institute for Endocrine and Metabolic Diseases | And 12 more authors.
International Journal of Molecular Medicine | Year: 2012

The aim of this study was to study the quantity change of endothelial progenitor cells (EPCs) in obese rats fed a high-fat-diet and to investigate the correlation of EPC numbers with visfatin. The impact of visfatin on the quantity and function of EPCs were further investigated by cell culture methods. Male Wistar rats were fed on either a standard diet (NC group) or a high-fat diet (HF group) for 16 weeks. Serum visfatin, Lee's index and the protein expression of visfatin in viseral adipose tissue (VAT) were determined. Bone marrow EPCs in 2 groups of rats were isolated, cultured and counted. EPCs primarily cultured from control male Wistar rats were treated with different concentrations of visfatin. The quantity, migration and adhesion capacity of EPCs were evaluated after visfatin treatment. Protein expression of nuclear factor-κB (NF-κB) in the nuclei of EPCs was detected. After 16-week feeding, body weight, serum visfatin, Lee's index and visfatin contents in viseral fat were significantly increased in the HF group compared with NC group (P<0.01 or P<0.05). The quantity of EPCs primarily cultured from rats in HF group was lower than that in NC group. The quantity of EPCs was negatively correlated with serum visfatin levels, visceral fat, fasting blood glucose, HOMA-IR, total cholesterol, triglyceride and body weight (P<0.01). In cultured EPCs, visfatin significantly increased the protein expression of NF-κB in EPC nuclei (P<0.01) in a dose-dependent manner. The migration and adhesion capacity were impaired by visfatin treatment (P<0.01). In conclusion, bone marrow-derived EPCs decrease in number and have impaired migration and adhesion function in high-fat-fed obese rats, along with increased serum visfatin and protein contents in VAT. Visfatin may have an impact on the quantity and function of EPCs through the NF-κB pathway. Source

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