Insulin resistance, serum adiponectin, and proinflammatory markers in young subjects with the metabolic syndrome

被引:53
作者
Kowalska, Irina [1 ]
Straczkowski, Marek [1 ]
Nikolajuk, Agnieszka [1 ]
Adamska, Agnieszka [1 ]
Karczewska-Kupczewska, Monika [1 ]
Otziomek, Elzbieta [1 ]
Kinalska, Ida [1 ]
Gorska, Maria [1 ]
机构
[1] Med Univ Bialystok, Dept Endocrinol Diabet & Internal Med, PL-15276 Bialystok, Poland
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 2008年 / 57卷 / 11期
关键词
D O I
10.1016/j.metabol.2008.06.008
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Insulin resistance is the underlying metabolic abnormality in the metabolic syndrome. The low-grade chronic inflammation may be associated with metabolic risk factors and atherogenesis. The aim of our study was to establish the link between the metabolic syndrome, as defined by the National Cholesterol Education program (NCEP) criteria, and insulin sensitivity, serum adiponectin, and parameters of chronic inflammation in young subjects. The group of 223 subjects (mean age, 25.86 +/- 5.49 years; body mass index, 28.04 +/- 6.91 kg/m2) was studied. Oral glucose tolerance test, euglycemic hyperinsulinemic clamp, and estimation of serum adiponectin and proinflammatory factors were performed. The NCEP-defined metabolic syndrome was present in 49 subjects (21.97%). The higher the number of NCEP criteria fulfilled was, the bigger were the decrease in insulin sensitivity (P <.0001) and adiponectin (P <.0001) and the increase in fasting and postload insulin (both Ps <.0001), C-reactive protein (P <.0001), interleukin IS (P <.0001), interleukin 6 (P <.0001), and Soluble tumor necrosis factor-a receptors sTNFRI (P <.0001) and sTNFR2 (P <.0001) observed. Multiple regression analysis revealed that adiponectin and inflammatory factors predicted NCEP score independent of insulin sensitivity (all adjusted beta values between .16 and .32, all Ps <.01). Young subjects with metabolic syndrome demonstrate an increased inflammatory response and lower adiponectin concentration. (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:1539 / 1544
页数:6
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