Sex-specific and sex-independent quantitative trait loci for facets of the metabolic syndrome in WOKW rats

被引:44
作者
Klöting, I [1 ]
Kovács, P [1 ]
van den Brandt, J [1 ]
机构
[1] Ernst Moritz Arndt Univ Greifswald, Dept Lab Anim Sci, Fac Med, D-17495 Karlsburg, Germany
关键词
genetics; chromosome; serum lipids; serum leptin; body weight;
D O I
10.1006/bbrc.2001.4932
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
WOKW rats develop a complete metabolic syndrome closely resembling human disease. Since genetic studies using male (WOKW x DA)FB progeny showed that several independent genetic factors were involved, a polygenic basis for the syndrome in WOKW was assumed. However, because the metabolic syndrome in human clearly demonstrates sex differences, we have extended our study to include both male and female (WOKW x DA)FS progeny in a genome-wide scan. Male- or female-specific quantitative trait loci (QTLs) were mapped for body weight, body mass index, adiposity index and serum insulin on chromosomes 1 and 5, serum triglycerides on chromosomes 4, 7, 11, and 16, serum total and high density lipoprotein cholesterol on chromosomes 3, 4, 5, 10, and 17, and serum leptin on chromosomes 8 and 16 as well as blood glucose and glucose tolerance (AUC) on chromosomes 3, 4 and 17. QTLs for both, males and females were only found for body weight on chromosome 1 and for serum total cholesterol on chromosome 3 and 10. These findings clearly demonstrate that there are sex-specific and sex-independent QTLs for facets of the metabolic syndrome in WOKW rats. (C) 2001 academic Press.
引用
收藏
页码:150 / 156
页数:7
相关论文
共 19 条
[1]   Identification of Cd36 (Fat) as an insulin-resistance gene causing defective fatty acid and glucose metabolism in hypertensive rats [J].
Aitman, TJ ;
Glazier, AM ;
Wallace, CA ;
Cooper, LD ;
Norsworthy, PJ ;
Wahid, FN ;
Al-Majali, KM ;
Trembling, PM ;
Mann, CJ ;
Shoulders, CC ;
Graf, D ;
St Lezin, E ;
Kurtz, TW ;
Kren, V ;
Pravenec, M ;
Ibrahimi, A ;
Abumrad, NA ;
Stanton, LW ;
Scott, J .
NATURE GENETICS, 1999, 21 (01) :76-83
[2]   Molecular pathology in the obese spontaneous hypertensive Koletsky rat: A model of Syndrome X [J].
Ernsberger, P ;
Koletsky, RJ ;
Friedman, JE .
THE METABOLIC SYNDROME X: CONVERGENCE OF INSULIN RESISTANCE, GLUCOSE INTOLERANCE, HYPERTENSION, OBESITY, AND DYSLIPIDEMIAS-SEARCHING FOR THE UNDERLYING DEFECTS, 1999, 892 :272-288
[3]  
Hunt KJ, 2000, GENET EPIDEMIOL, V19, P395, DOI 10.1002/1098-2272(200012)19:4<395::AID-GEPI10>3.0.CO
[4]  
2-3
[5]   Identification of quantitative trait loci for serum cholesterol levels in stroke-prone spontaneously hypertensive rats [J].
Kato, N ;
Tamada, T ;
Nabika, T ;
Ueno, K ;
Gotoda, T ;
Matsumoto, C ;
Mashimo, T ;
Sawamura, M ;
Ikeda, K ;
Nara, Y ;
Yamori, Y .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2000, 20 (01) :223-229
[6]  
Klimes Iwar, 1995, Blood Pressure, V4, P137, DOI 10.3109/08037059509077585
[7]  
KLOTING I, 1995, J EXP ANIM SCI, V37, P42
[8]  
KLOTING I, 1991, DIABETES RES CLIN EX, V18, P79
[9]   Quantitative trait loci on chromosomes 1 and 4 affect lipid phenotypes in the rat [J].
Kovács, P ;
Klöting, I .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1998, 354 (01) :139-143
[10]   Genetic dissection of the syndrome X in the rat [J].
Kovács, P ;
van den Brandt, J ;
Klöting, I .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2000, 269 (03) :660-665