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Articles by C. Liu
Total Records ( 3 ) for C. Liu
  M. Song , W. Han , H. Bao , C. Liu , C. Wu and C. Zhao
  In the present study, embryo liver tissues collected from hypoxic incubation of Tibet chicken and Shouguang chicken were analyzed on their histological structures and antioxidant capacity as well as differential proteomics to study the mechanism of Tibet chicken’s adaptability to hypoxia. The results of histological study conducted with paraffin and ultrathin sections showed that Shouguang chicken had a weaker liver structure with less cell layers and the development of its liver was more impaired compared with Tibet chicken and Tibet chicken maintained relatively better mitochondria than Shouguang chicken. The content of Maleic dialdehyde in Tibet chicken was lower than Shougguang chicken, but the total antioxidant capacity and the content of Superoxide Dismutase in Tibet chicken were higher than Shouguang chicken. Using two-dimensional electrophoresis and mass spectrometry, we identified 8 differential expression liver proteins between Tibet chicken and Shouguang chicken, in which 6 proteins (enolase I, pyruvate dehydrogenase, ATP synthase, ubiquinol-cytochrome C reductase, superoxide dismutase and apolipoprotein A-I) showed higher expression level in Tibet chicken than that in Shouguang chicken while the expressions of the other 2 proteins (Triose phosphate isomerase, adenosine 5-diphosphosugar pyrophosphatase) were less in livers of Tibet chicken. These results indicated that Tibet chicken had higher glucose oxidation level, electron transfer efficiency and antioxidant ability than Shouguang chicken under the hypoxic condition and these differences made Tibet chicken have better adaptability to hypoxia than Lowland chicken. The study made a good basis for the further study of the genetic mechanism of adaptation to hypoxia.
  L. Chen , Q. Li , Z. Yang , Z. Ye , Y. Huang , M. He , J. Wen , X. Wang , B. Lu , J. Hu , C. Liu , C. Ling , S. Qu and R. Hu
  Aim  To assess the relationship between serum total osteocalcin and measurements of adiposity, glucose tolerance, lipid profile, adipokine and chronic low-grade inflammation in middle-aged and elderly Chinese subjects.

Methods  We performed a cross-sectional community-based study in central Shanghai. Serum total osteocalcin was measured by radioimmunoassay in 783 men and 946 post-menopausal women. Their associations with measurements of adiposity, glucose tolerance, lipid profile and chronic low-grade inflammation were examined.

Results  Serum total osteocalcin levels revealed a sexual dimorphism, with post-menopausal women having significantly higher levels than men (< 0.001). Serum osteocalcin levels of participants with self-reported cardiovascular disease were significantly lower (= 0.044) than those without. In men, serum osteocalcin levels of participants with the metabolic syndrome were significantly lower than those without the metabolic syndrome (= 0.036). Serum osteocalcin correlated negatively with fasting serum insulin, homeostasis model assessment of insulin resistance, alanine aminotransferase, triglycerides and total cholesterol, and positively with homeostasis model assessment of β-cell function in both men and post-menopausal women (all < 0.05). In men, serum osteocalcin correlated negatively with BMI, diastolic blood pressure, fasting plasma glucose and 2-h oral glucose tolerance test glucose after adjustment for age (all < 0.05). In post-menopausal women, serum osteocalcin correlated negatively with waist-hip ratio, LDL cholesterol and C-reactive protein, and positively with adiponectin (all < 0.05). Serum osteocalcin was not associated with CXC chemokine ligand 5 level (> 0.05). Alanine aminotransferase was an independent predictor of serum osteocalcin in both men and post-menopausal women (both < 0.001). Adiponectin was an independent predictor of serum osteocalcin in post-menopausal women (= 0.011). Serum osteocalcin was an independent predictor of homeostasis model assessment of β-cell function in both genders (both < 0.05).

Conclusions

  C. Liu , X. Wang , Z. Chen , L. Zhang , Y. Wu and Y. Zhang
 

Background: The effects of hepatic ischemia-reperfusion (I/R) on insulin signaling remain unclear. We observed changes in insulin secretion and signal protein expression during the early steps in insulin signaling after hepatic I/R in rats.

Materials and Methods: Eighty healthy Wistar rats were randomly divided into an I/R group and a control (C) group. After we exposed the hepatic hilum, ischemia was induced by clamping the hepatic artery and portal vein for 30 minutes and then the liver was reperfused for 2 hours in the I/R group; a show procedure was done in the C group. Blood samples were obtained after exposure of the hepatic hilum (T1) and 2 hours after reperfusion in the I/R group (T2) and 2.5 hours after T1 in the C group (T2). We measured glucose and insulin plasma concentrations. We determined the expressions of insulin signaling proteins, including insulin receptor (IR) β unit (IR β), IR substrate 1 (IRS-1), IRS-2, and P85 in phosphatidylinositol 3-kinase (PI3K) and tyrosine phosphorylation of these proteins in liver and skeletal muscle.

Results: Plasma glucose concentrations increased in both groups at T2 (P < .01) and were higher in the I/R group (P < .01). Insulin concentrations in the I/R group did not change significantly at T2. Insulin concentrations at T2 were higher than those at T1 in the C group (P < .05). Expressions of insulin signal proteins showed no significant difference between the 2 groups; however, tyrosine phosphorylation of IR β, IRS-1, IRS-2, and the interactions between IRS-1 in skeletal muscle or IRS-2 in liver and PI3K were significantly lower in the I/R group than the C group.

Conclusion: Hepatic I/R inhibited insulin secretion and induced insulin resistance via down-regulation during the early steps in insulin signaling in rats.
 
 
 
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