Chagnon Y C, Pérusse L, Lamothe M, Chagnon M, Nadeau A, Dionne F T, Gagnon J, Chung W K, Leibel R L, Bouchard C
Physical Activity Sciences Laboratory, Laval University, Ste-Foy, Québec, Canada.
Obes Res. 1997 Mar;5(2):115-21. doi: 10.1002/j.1550-8528.1997.tb00651.x.
A single-gene rodent mutation (diabetes) and a quantitative trait locus (dietary obese 1) mapped to the mid portion of mouse chromosome 4 have been related to obesity and/or insulin levels. Synteny relationships place their putative human homologs on 1p31 and 1p35-p31, respectively. In 137 sibships of adult brothers and sisters from the Québec Family Study, genetic linkages between seven microsatellite markers from 1p32-p22 and various obesity- and diabetes-related quantitative phenotypes were examined using single locus sibpair linkage analysis. Suggestive linkages were observed between markers D1S476 and body mass index (p = 0.05), fat mass (p = 0.02), the sum of six skinfolds (p = 0.02), the insulin area after an oral glucose tolerance test (p = 0.02), and between the neighboring marker D1S200 and body mass index (p = 0.03), and fat mass (p = 0.009). Suggestive linkages were also observed between the more telomeric markers D1S193 and body mass index (p = 0.03), and between the neighboring marker D1S197 and fasting insulin level (p = 0.05). No linkage was observed with the trunk to extremity skinfolds ratio. These linkages suggest that human homologs of the mouse diabetes or dietary obese 1 and/or other genes in this interval on chromosome 1 play a role in the regulation of body mass, body composition, and insulin levels, but not of subcutaneous fat distribution.
一种单基因啮齿动物突变（糖尿病）和一个定位到小鼠4号染色体中部的数量性状基因座（饮食性肥胖1）已被证明与肥胖和/或胰岛素水平有关。同线关系分别将它们假定的人类同源基因定位在1p31和1p35 - p31。在魁北克家庭研究的137对成年兄弟姐妹同胞对中，使用单基因座同胞对连锁分析研究了来自1p32 - p22的7个微卫星标记与各种肥胖和糖尿病相关数量性状之间的遗传连锁。在标记D1S476与体重指数（p = 0.05）、脂肪量（p = 0.02）、六项皮褶厚度之和（p = 0.02）、口服葡萄糖耐量试验后的胰岛素面积（p = 0.02）之间，以及相邻标记D1S200与体重指数（p = 0.03）和脂肪量（p = 0.009）之间观察到提示性连锁。在更靠近端粒的标记D1S193与体重指数（p = 0.03）之间，以及相邻标记D1S197与空腹胰岛素水平（p = 0.05）之间也观察到提示性连锁。未观察到与躯干与四肢皮褶厚度比值的连锁。这些连锁表明，小鼠糖尿病或饮食性肥胖1的人类同源基因和/或1号染色体上该区间的其他基因在体重、身体成分和胰岛素水平的调节中起作用，但在皮下脂肪分布的调节中不起作用。
