A genome-wide scan for quantitative trait loci linked to obesity phenotypes among West Africans

被引:29
作者
Chen, G
Adeyemo, AA
Johnson, T
Zhou, J
Amoah, A
Owusu, S
Acheampong, J
Agyenim-Boateng, K
Eghan, BA
Oli, J
Okafor, G
Abbiyesuku, F
Dunston, GM
Chen, Y
Collins, F
Rotimi, C
机构
[1] Howard Univ, Coll Med, Natl Human Genome Ctr, Genet Epidemiol Unit, Washington, DC 20059 USA
[2] Univ Ibadan, Coll Med, Ibadan, Nigeria
[3] Univ Lagos, Coll Med, Endocrine & Metab Unit, Lagos, Nigeria
[4] Univ Ghana, Sch Med, Dept Med, Accra, Ghana
[5] Univ Sci & Technol, Dept Med, Kumasi, Ghana
[6] Univ Nigeria, Teaching Hosp, Dept Med, Enugu, Nigeria
[7] NHGRI, NIH, Bethesda, MD 20892 USA
关键词
genome scan; type; 2; diabetes; genetics; West Africa;
D O I
10.1038/sj.ijo.0802873
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
OBJECTIVE: To identify quantitative trait loci (QTL) for three obesity phenotypes: body mass index (BMI), fat mass (FM) and percent body fat (PBF) in West Africans with type 2 diabetes (T2DM). DESIGN: An affected sibling pair (ASP) design, in which both siblings had T2DM. Obesity was analyzed as a quantitative trait using a variance components approach. SUBJECTS: Sib-pairs affected with T2DM from the Africa America Diabetes Mellitus (AADM) study, comprising 321 sibling pairs and 36 half-sibling pairs. MEASUREMENTS: Weight was measured on an electronic scale to the nearest 0.1 kg, and height was measured with a stadiometer to the nearest 0.1 cm. Body composition was estimated using bioelectric impedance analysis (BIA). Genotyping was carried out at the Center for Inherited Disease Research (CIDR) with a panel of 390 trinucleotide and tetranucleotide repeats. RESULTS: The obesity-related phenotype showing the strongest linkage evidence was PBF on chromosome 2 (LOD 3.30 at 72.6 cM, marker D2S739). Suggestive linkage to FM was found on chromosomes 2 (LOD 2.56 at 80.4 cM) and 5 (LOD 2.25 at 98 cM, marker D5S1725). The highest LOD score for BMI was 1.68 (chromosome 4, 113.8 cM). The areas of linkage for the three phenotypes showed some clustering as all three phenotypes were linked to the same regions of 2p13 and 5q14, and our study replicated linkage evidence for several regions previously reported in other studies. CONCLUSION: We obtained evidence for several QTLs on chromosome 2, 4 and 5 to three obesity phenotypes. This study provides data on the genetics of obesity in populations that are currently under represented in the global effort directed at understanding the pathophysiology of excess adiposity in free living individuals.
引用
收藏
页码:255 / 259
页数:5
相关论文
共 25 条
[1]   Merlin-rapid analysis of dense genetic maps using sparse gene flow trees [J].
Abecasis, GR ;
Cherny, SS ;
Cookson, WO ;
Cardon, LR .
NATURE GENETICS, 2002, 30 (01) :97-101
[2]   A genome-wide scan for body mass index among Nigerian families [J].
Adeyemo, A ;
Luke, A ;
Cooper, R ;
Wu, XD ;
Tayo, B ;
Zhu, XF ;
Rotimi, C ;
Bouzekri, N ;
Ward, R .
OBESITY RESEARCH, 2003, 11 (02) :266-273
[3]  
*AM DIAB ASS, 1999, DIABETES CARE, V22, pS20
[4]  
Blair SN, 2002, MAYO CLIN PROC, V77, P109
[5]  
CARDON LR, 1994, AM J HUM GENET, V55, P825
[6]  
*CAS W RES U CTR E, 2000, SAGE STAT AN GEN EP
[7]   The human obesity gene map:: The 2002 update [J].
Chagnon, YC ;
Rankinen, T ;
Snyder, EE ;
Weisnagel, SJ ;
Pérusse, LK ;
Bouchard, C .
OBESITY RESEARCH, 2003, 11 (03) :313-367
[8]   A major quantitative trait locus determining serum leptin levels and fat mass is located on human chromosome 2 [J].
Comuzzie, AG ;
Hixson, JE ;
Almasy, L ;
Mitchell, BD ;
Mahaney, MC ;
Dyer, TD ;
Stern, MP ;
MacCluer, JW ;
Blangero, J .
NATURE GENETICS, 1997, 15 (03) :273-276
[9]   The search for human obesity genes [J].
Comuzzie, AG ;
Allison, DB .
SCIENCE, 1998, 280 (5368) :1374-1377
[10]   The genetic basis of plasma variation in adiponectin, a global endophenotype for obesity and the metabolic syndrome [J].
Comuzzie, AG ;
Funahashi, T ;
Sonnenberg, G ;
Martin, LJ ;
Jacob, HJ ;
Black, AEK ;
Maas, D ;
Takahashi, M ;
Kihara, S ;
Tanaka, S ;
Matsuzawa, Y ;
Blangero, J ;
Cohen, D ;
Kissebah, A .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2001, 86 (09) :4321-4325