目的探讨初诊肥胖2型糖尿病患者血清Betatrophin水平与胰岛β细胞功能的关系。方法方便选择2014年1月—2015年1月初诊肥胖2型糖尿病患者100例为研究对象(观察组),另选择同期该院体检健康者(NGT)者100名为对照观察(对照组)。测量人体指标...目的探讨初诊肥胖2型糖尿病患者血清Betatrophin水平与胰岛β细胞功能的关系。方法方便选择2014年1月—2015年1月初诊肥胖2型糖尿病患者100例为研究对象(观察组),另选择同期该院体检健康者(NGT)者100名为对照观察(对照组)。测量人体指标,检测相关代谢血生化指标,采用酶联免疫吸附实验(ELISA)法测定空腹血清Betatrophin水平,采用直线相关分析研究betatrophin与胰岛β细胞功能、体测及代谢指标的相关关系。结果观察组血清Betatrophin水平(422.5±247.60)pg/m L明显高于对照组(316.3±293.30)pg/m L,差异有统计学意义(P<0.05);相关性分析提示Betatrophin与腰臀比、HOMA-IR、FPG、2 h PG、HbA1c、FINS、TG呈正相关(r=0.215、0.216、0.249、0.447、0.338、0.452、0.470,P<0.01),与HDL-C、HOMA-β成负相关(r=-0.256、-0.363,P<0.05),差异有统计学意义(P<0.05)。结论初诊肥胖2型糖尿病患者的血清betatrophin水平较NGT组明显升高,并且与胰岛β细胞功能密切相关,推测其参与了糖尿病的发生。展开更多
AIM: To investigate the diagnostic utility of beta 2 microglobulin (B2-M) levels and analyze this correlation with the activity of inflammatory bowel disease (IBD).
This study aimed to explore the mechanism of a novel mutation （p.Lys38Glu） in apolipoprotein H （APOH） gene causing hereditary beta2-glycoprotein I （β2GPI） deficiency and thrombosis in a proband with thrombophil...This study aimed to explore the mechanism of a novel mutation （p.Lys38Glu） in apolipoprotein H （APOH） gene causing hereditary beta2-glycoprotein I （β2GPI） deficiency and thrombosis in a proband with thrombophilia. The plasma level of β2GPI was measured by ELISA and Western blotting, and anti-β2GPI antibody by ELISA. Lupus anticoagulant （LA） was assayed using the dilute Russell viper venom time. Deficiency of the major natural anticoagulants including protein C （PC）, protein S （PS）, antithrombin （AT） and thrombomodulin （TM） was excluded from the proband. A mutation analysis was performed by amplification and sequencing of the APOH gene. Wild type and mutant （c.112A〉G） APOH expression plasmids were constructed and transfected into HEK293T cells. The results showed that the thrornbin generation capacity of the proband was higher than that of the other family members. Missense mutation p.Lys38Glu in APOH gene and LA coexisted in the proband. The mutation led to β2GPI deficiency and thrombosis by impairing the protein production and inhibiting the platelet aggregation. It was concluded that the recurrent thrombosis of the proband is associated with the coexistence ofp.Lys38Glu mutation in APOH gene and LA in plasma.展开更多
基金Supported by the National Natural Science Foundation of China(No.51572232,No.51561135015)Key Technology Research and Development Program of Ningbo(No.2011B1001)
文摘目的探讨初诊肥胖2型糖尿病患者血清Betatrophin水平与胰岛β细胞功能的关系。方法方便选择2014年1月—2015年1月初诊肥胖2型糖尿病患者100例为研究对象(观察组),另选择同期该院体检健康者(NGT)者100名为对照观察(对照组)。测量人体指标,检测相关代谢血生化指标,采用酶联免疫吸附实验(ELISA)法测定空腹血清Betatrophin水平,采用直线相关分析研究betatrophin与胰岛β细胞功能、体测及代谢指标的相关关系。结果观察组血清Betatrophin水平(422.5±247.60)pg/m L明显高于对照组(316.3±293.30)pg/m L,差异有统计学意义(P<0.05);相关性分析提示Betatrophin与腰臀比、HOMA-IR、FPG、2 h PG、HbA1c、FINS、TG呈正相关(r=0.215、0.216、0.249、0.447、0.338、0.452、0.470,P<0.01),与HDL-C、HOMA-β成负相关(r=-0.256、-0.363,P<0.05),差异有统计学意义(P<0.05)。结论初诊肥胖2型糖尿病患者的血清betatrophin水平较NGT组明显升高,并且与胰岛β细胞功能密切相关,推测其参与了糖尿病的发生。
文摘AIM: To investigate the diagnostic utility of beta 2 microglobulin (B2-M) levels and analyze this correlation with the activity of inflammatory bowel disease (IBD).
文摘This study aimed to explore the mechanism of a novel mutation （p.Lys38Glu） in apolipoprotein H （APOH） gene causing hereditary beta2-glycoprotein I （β2GPI） deficiency and thrombosis in a proband with thrombophilia. The plasma level of β2GPI was measured by ELISA and Western blotting, and anti-β2GPI antibody by ELISA. Lupus anticoagulant （LA） was assayed using the dilute Russell viper venom time. Deficiency of the major natural anticoagulants including protein C （PC）, protein S （PS）, antithrombin （AT） and thrombomodulin （TM） was excluded from the proband. A mutation analysis was performed by amplification and sequencing of the APOH gene. Wild type and mutant （c.112A〉G） APOH expression plasmids were constructed and transfected into HEK293T cells. The results showed that the thrornbin generation capacity of the proband was higher than that of the other family members. Missense mutation p.Lys38Glu in APOH gene and LA coexisted in the proband. The mutation led to β2GPI deficiency and thrombosis by impairing the protein production and inhibiting the platelet aggregation. It was concluded that the recurrent thrombosis of the proband is associated with the coexistence ofp.Lys38Glu mutation in APOH gene and LA in plasma.
