Serum resistin level in essential hypertension patients with different glucose tolerance

被引:50
作者
Zhang, JL
Qin, YW
Zheng, X
Qiu, JL
Zou, DJ
机构
[1] Changhai Hosp, Dept Cardiol, Shanghai 200433, Peoples R China
[2] Changhai Hosp, Dept Endocrinol, Shanghai 200433, Peoples R China
关键词
blood glucose; hypertension; resistin;
D O I
10.1046/j.1464-5491.2003.01057.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Aims To investigate resistin concentrations in patients with essential hypertension and different glucose tolerance and the relationship between serum resistin level and blood glucose. Methods Sixty-five patients with essential hypertension [13 with Type 2 diabetes mellitus (DM), 26 with impaired glucose tolerance (IGT), and 26 with normal glucose tolerance (NGT); 30 males, 35 females] were studied. Fasting serum resistin concentrations were measured by enzyme immunoassay (EIA). Oral glucose tolerance tests and insulin release tests were used to calculate glucose area under the curve (AUC(G)), the ratio of insulin to glucose (DeltaI(30)/DeltaG(30)), and insulin sensitivity index (ISI) according to Cederholm's formula. Results Fasting serum resistin concentrations (mug/l) in DM (34.9 +/- 10.2) patients were significantly higher than those in IGT (25.1 +/- 10.4) (P < 0.05) and in NGT (21.5 +/- 7.9) (P < 0.05) patients. Pearson correlation showed that fasting serum resistin concentration was correlated with AUC(G) (r = 0.445, P < 0.001), ISI (r = - 0.322, P < 0.01) and DeltaI(30) /DeltaG(30) ( r = - 0.366, P < 0.01), but not body mass index and waist-hip ratio. After adjustment for gender, age and body mass index (BMI), partial correlation analysis showed that the fasting serum resistin concentrations were still correlated with AUC(G) (r = 0.327, P < 0.01) and DeltaI(30) /DeltaG(30) ( r = - 0.348, P < 0.01), but ISI. Conclusion Resistin may be involved in the development of diabetes in humans.
引用
收藏
页码:828 / 831
页数:4
相关论文
共 10 条
[1]   INSULIN RELEASE AND PERIPHERAL SENSITIVITY AT THE ORAL GLUCOSE-TOLERANCE TEST [J].
CEDERHOLM, J ;
WIBELL, L .
DIABETES RESEARCH AND CLINICAL PRACTICE, 1990, 10 (02) :167-175
[2]   THE TRIUMVIRATE - BETA-CELL, MUSCLE, LIVER - A COLLUSION RESPONSIBLE FOR NIDDM [J].
DEFRONZO, RA .
DIABETES, 1988, 37 (06) :667-687
[3]   DECREASED INSULIN-SECRETION AND INCREASED INSULIN-RESISTANCE ARE INDEPENDENTLY RELATED TO THE 7-YEAR RISK OF NIDDM IN MEXICAN-AMERICANS [J].
HAFFNER, SM ;
MIETTINEN, H ;
GASKILL, SP ;
STERN, MP .
DIABETES, 1995, 44 (12) :1386-1391
[4]  
Jonke J, 2002, OBES RES, V10, P1
[5]   Resistin, central obesity, and type 2 diabetes [J].
McTernan, CL ;
McTernan, PG ;
Harte, AL ;
Levick, PL ;
Barnett, AH ;
Kumar, S .
LANCET, 2002, 359 (9300) :46-47
[6]   Increased resistin gene and protein expression in human abdominal adipose tissue [J].
McTernan, PG ;
McTernan, CL ;
Chetty, R ;
Jenner, K ;
Fisher, FM ;
Lauer, M ;
Crocker, J ;
Barnett, AH ;
Kumar, S .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2002, 87 (05) :2407-2410
[7]  
Moller L F, 1995, J Cardiovasc Risk, V2, P339
[8]   Insulin resistance and Type 2 diabetes are not related to resistin expression in human fat cells or skeletal muscle [J].
Nagaev, I ;
Smith, U .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2001, 285 (02) :561-564
[9]   ROLE OF INSULIN RESISTANCE IN HUMAN-DISEASE [J].
REAVEN, GM .
DIABETES, 1988, 37 (12) :1595-1607
[10]   The hormone resistin links obesity to diabetes [J].
Steppan, CM ;
Bailey, ST ;
Bhat, S ;
Brown, EJ ;
Banerjee, RR ;
Wright, CM ;
Patel, HR ;
Ahima, RS ;
Lazar, MA .
NATURE, 2001, 409 (6818) :307-312