Relationship between serum levels of C-reactive protein and α1-antitrypsin and insulin resistance in obese women.

被引:0
作者
Ramirez Alvarado, Maria Matilde [1 ]
Sanchez Roitz, Cesar [2 ]
机构
[1] Univ Carabobo, Fac Ciencias Salud, Dept Bioquim, Escuela Ciencias Biomed & Tecnol, Valencia, Venezuela
[2] Ctr Med Dr Rafael Guerra Mendez, Lab Clin Cesar Sanchez Font, Valencia, Venezuela
来源
INVESTIGACION CLINICA | 2014年 / 55卷 / 03期
关键词
C reactive protein; alpha l-antitrypsin; insulin resistance; obesity; ACUTE-PHASE PROTEINS; CARDIOVASCULAR-DISEASE; GLUCOSE-TOLERANCE; INFLAMMATION; POPULATION; MECHANISMS; EXPRESSION; CYTOKINES; RESPONSES;
D O I
暂无
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Adipose tissue produces cytokines involved in insulin resistance (IR) such as IL-6, IL-8, TNF-a and proinflammatory molecules such as C reactive protein (CRP). alpha l-antitrypsin is an inflammation-sensitive plasma protein. The objective of this study is to determine the correlation between serum CRP high-sensitivity (CRPhs) and al-antitrypsin levels with IR indices in obese Venezuelan women. The study population consisted of 15 normal weight women (BMI 21.8 +/- 1.9 kg/m(2)) and 15 obese women (BMI 35.3 +/- 5.3 kg/m(2)). Obese and lean women underwent a 2 h-75g oral glucose tolerance test and the following indices were calculated: homeostatic model assessment of insulin resistance (HOMA-IR), homeostatic model assessment of cell function (HOMA-beta), Matsuda Index and Insulinogenic Index. The relationship between serum CRPhs and alpha 1-antitrypsin levels and these indices were determined. Obese women had higher CRPhs levels (p = 0.001) compared with normal weight women. In obese women, serum CRPhs levels were positively correlated with HOMA-IR (r=0.73, p=0.0021), HOMA-beta (r=0.53, p=0.031) and negatively correlated with the Matsuda Index (r= -0.60, p=0.017). No correlation between serum levels of a 1-antitrypsin and IR indices in the obese group and the lean group was observed. There was a relation between serum CRPhs levels and insulin resistance, suggesting a role of subclinical inflammation in IR.
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页码:249 / 259
页数:11
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