Jun Gyungah, Song Yeunjoo, Stein Catherine M, Iyengar Sudha K
Department of Epidemiology and Biostatistics, Case Western Reserve University, 2500 MetroHealth Drive, Cleveland, Ohio, USA.
BMC Genet. 2003 Dec 31;4 Suppl 1(Suppl 1):S8. doi: 10.1186/1471-2156-4-S1-S8.
A genome-wide screen was conducted for type 2 diabetes progression genes using measures of elevated fasting glucose levels as quantitative traits from the offspring enrolled in the Framingham Heart Study. We analyzed young (20-34 years) and old (>or= 35 years) subjects separately, using single-point and multipoint sibpair analysis, because of the possible differential impact of progression on the groups of interest. We observed significant linkage with change in fasting glucose levels on 1q25-32 (p = 5.21 x 10(-8)), 3p26.3-21.31 (p = 1 x 10(-11)), 8q23.1-24.13 (p = 2.94 x 10(-6)), 9p24.1-21.3 (p = 7 x 10(-7)), and 18p11.31-q22.1 (p < 10(-11)). The evidence for linkage on chromosomes 8 and 18 was consistent for the subset of study participants aged 43 through 55 years.
利用弗雷明汉心脏研究中纳入的后代的空腹血糖水平升高指标作为数量性状,对2型糖尿病进展基因进行了全基因组筛查。由于进展对感兴趣组可能存在不同影响,我们分别使用单点和多点同胞对分析,对年轻(20 - 34岁)和老年(≥35岁)受试者进行了分析。我们观察到在1q25 - 32(p = 5.21×10⁻⁸)、3p26.3 - 21.31(p = 1×10⁻¹¹)、8q23.1 - 24.13(p = 2.94×10⁻⁶)、9p24.1 - 21.3(p = 7×10⁻⁷)和18p11.31 - q22.1(p < 10⁻¹¹)区域,空腹血糖水平变化存在显著连锁。对于年龄在43至55岁的研究参与者子集,8号和18号染色体上的连锁证据是一致的。