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Genetics of Obesity and Type 2 Diabetes in African Americans

DOI: 10.1155/2013/396416

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Abstract:

Obesity and type 2 diabetes are highly prevalent and lead to significant morbidity and mortality. In the United States, the impact of these conditions may be worse on historically underserved minorities, particularly African Americans. Genetic ancestry and differences in physiology are unlikely to be the sole or primary determinants of these disparities. In addition, research in this area has the ethically problematic possibility of conflating race with biology. Despite these important considerations and the challenges of conducting this work, population-based approaches for investigating the etiology of obesity and T2D may yield useful information about the pathophysiology of disease, and have implications that extend to all affected individuals. The purpose of this paper is to describe what is understood about the genetic variation that underlies obesity and T2D in African Americans and other individuals of more recent African descent and to highlight several examples that illustrate how ensuring adequate minority representation in genetic research improves its quality. For a variety of reasons a number of unique insights have been possible as a result of these efforts. 1. Introduction In this paper, we will use the previously formulated definition of race by the Endocrinology Society’s 2012 consensus statement on health disparities in endocrine disorders as a “complex multidimensional construct reflecting the confluence of biological factors and geographical origins, culture, economic, political, and legal factors, as well as racism” [1]. As described in more detail below, in genetic research, individuals are often grouped on the basis of markers of ancestry and admixture; these delineations may help to address the important problem of population stratification in association studies. Results are frequently reported with respect to commonly used racial designations, a practice that is intended to make findings understandable and generalizable, but that may fail to appropriately emphasize the distinction between race and biology. A full discussion of the methodological and ethical issues involved in using racial categories in genetic research is beyond the scope of this paper; the reader is referred to a number of excellent papers on this topic [2]. A multidisciplinary working group previously convened to address this issue emphasized that each individual has characteristics that could form the basis for his or her membership in any number of populations [3]. This group recommended that, in research publications, methodology should be clear and

References

[1]  D. R. Williams, “Race and health: basic questions, emerging directions,” Annals of Epidemiology, vol. 7, no. 5, pp. 322–333, 1997.
[2]  S. E. Ali-Khan, T. Krakowski, R. Tahir, and A. S. Daar, “The use of race, ethnicity and ancestry in human genetic research,” The HUGO Journal, vol. 5, no. 1–4, pp. 47–63, 2011.
[3]  S. Olson, K. Berg, V. Bonham et al., “The use of racial, ethnic, and ancestral categories in human genetics research,” American Journal of Human Genetics, vol. 77, no. 4, pp. 519–532, 2005.
[4]  S. M. Fullerton, J. H. Yu, J. Crouch, K. Fryer-Edwards, and W. Burke, “Population description and its role in the interpretation of genetic association,” Human Genetics, vol. 127, no. 5, pp. 563–572, 2010.
[5]  R. S. Cooper, B. Tayo, and X. Zhu, “Genome-wide association studies: implications for multiethnic samples,” Human Molecular Genetics, vol. 17, R2, pp. R151–R155, 2008.
[6]  A. P. Morris, “Transethnic meta-analysis of genomewide association studies,” Genetic Epidemiology, vol. 35, no. 8, pp. 809–822, 2011.
[7]  J. Fu, E. A. Festen, and C. Wijmenga, “Multi-ethnic studies in complex traits,” Human Molecular Genetics, vol. 20, R2, pp. R206–R213, 2011.
[8]  N. A. Rosenberg, L. Huang, E. M. Jewett, Z. A. Szpiech, I. Jankovic, and M. Boehnke, “Genome-wide association studies in diverse populations,” Nature Reviews Genetics, vol. 11, no. 5, pp. 356–366, 2010.
[9]  Y. Y. Teo, K. S. Small, and D. P. Kwiatkowski, “Methodological challenges of genome-wide association analysis in Africa,” Nature Reviews Genetics, vol. 11, no. 2, pp. 149–160, 2010.
[10]  M. W. Foster and R. R. Sharp, “Beyond race: towards a whole-genome perspective on human populations and genetic variation,” Nature Reviews Genetics, vol. 5, no. 10, pp. 790–796, 2004.
[11]  S. A. Tishkoff, F. A. Reed, F. R. Friedlaender et al., “The genetic structure and history of Africans and African Americans,” Science, vol. 324, no. 5930, pp. 1035–1044, 2009.
[12]  A. D. Johnson, R. E. Handsaker, S. L. Pulit, M. M. Nizzari, C. J. O'Donnell, and P. I. W. De Bakker, “SNAP: a web-based tool for identification and annotation of proxy SNPs using HapMap,” Bioinformatics, vol. 24, no. 24, pp. 2938–2939, 2008.
[13]  S. Bollepalli, L. M. Dolan, R. Deka, and L. J. Martin, “Association of FTO gene variants with adiposity in African-American adolescents,” Obesity, vol. 18, no. 10, pp. 1959–1963, 2010.
[14]  G. Liu, H. Zhu, V. Lagou et al., “FTO variant rs9939609 is associated with body mass index and waist circumference, but not with energy intake or physical activity in European- and African-American youth,” BMC Medical Genetics, vol. 11, no. 1, article 57, 2010.
[15]  M. R. Wing, J. Ziegler, C. D. Langefeld et al., “Analysis of FTO gene variants with measures of obesity and glucose homeostasis in the IRAS Family Study,” Human Genetics, vol. 125, no. 5-6, pp. 615–626, 2009.
[16]  M. R. Wing, J. M. Ziegler, C. D. Langefeld et al., “Analysis of FTO gene variants with obesity and glucose homeostasis measures in the multiethnic Insulin Resistance Atherosclerosis Study cohort,” International Journal of Obesity, vol. 35, no. 9, pp. 1173–1182, 2011.
[17]  Z. Lombard, N. J. Crowther, L. van der Merwe, P. Pitamber, S. A. Norris, and M. Ramsay, “Appetite regulation genes are associated with body mass index in black South African adolescents: a genetic association study,” BMJ Open, vol. 2, no. 3, 2012.
[18]  M. T. Hassanein, H. N. Lyon, T. T. Nguyen et al., “Fine mapping of the association with obesity at the FTO locus in African-derived populations,” Human Molecular Genetics, vol. 19, no. 14, Article ID ddq178, pp. 2907–2916, 2010.
[19]  A. Adeyemo, G. Chen, J. Zhou et al., “FTO genetic variation and association with obesity in West Africans and African Americans,” Diabetes, vol. 59, no. 6, pp. 1549–1554, 2010.
[20]  S. F. A. Grant, M. Li, J. P. Bradfield et al., “Association analysis of the FTO gene with obesity in children of Caucasian and African ancestry reveals a common tagging SNP,” PLoS ONE, vol. 3, no. 3, Article ID e1746, 2008.
[21]  J. M. Hester, M. R. Wing, J. Li et al., “Implication of European-derived adiposity loci in African Americans,” International Journal of Obesity, vol. 36, no. 3, pp. 465–473, 2012.
[22]  A. Scuteri, S. Sanna, W. M. Chen et al., “Genome-wide association scan shows genetic variants in the FTO gene are associated with obesity-related traits,” PLoS Genetics, vol. 3, no. 7, article e115, 2007.
[23]  S. A. Tishkoff and K. K. Kidd, “Implications of biogeography of human populations for ‘race’ and medicine,” Nature Genetics, vol. 36, no. 11, pp. S21–S27, 2004.
[24]  J. Asimit, A. Day-Williams, L. Zgaga, I. Rudan, V. Boraska, and E. Zeggini, “An evaluation of different meta-analysis approaches in the presence of allelic heterogeneity,” European Journal of Human Genetics, vol. 20, no. 6, pp. 709–712, 2012.
[25]  X. Wang, X. Liu, X. Sim et al., “A statistical method for region-based meta-analysis of genome-wide association studies in genetically diverse populations,” European Journal of Human Genetics, vol. 20, no. 4, pp. 469–475, 2012.
[26]  L. Yun, C. Willer, S. Sanna, and G. Abecasis, “Genotype imputation,” Annual Review of Genomics and Human Genetics, vol. 10, pp. 387–406, 2009.
[27]  L. Huang, M. Jakobsson, T. J. Pemberton et al., “Haplotype variation and genotype imputation in African populations,” Genetic Epidemiology, vol. 35, no. 8, pp. 766–780, 2011.
[28]  G. R. Abecasis, A. Auton, L. D. Brooks et al., “An integrated map of genetic variation from 1,092 human genomes,” Nature, vol. 491, no. 7422, pp. 56–65, 2012.
[29]  X. Gao, T. Haritunians, P. Marjoram et al., “Genotype imputation for latinos using the HapMap and 1000 genomes project reference panels,” Frontiers in Genetics, vol. 3, article 117, 2012.
[30]  S. H. Golden, A. Brown, J. A. Cauley et al., “Health disparities in endocrine disorders: biological, clinical, and nonclinical factors—an endocrine society scientific statement,” The Journal of Clinical Endocrinology and Metabolism, vol. 97, no. 9, pp. E1579–E1639, 2012.
[31]  J. Marchini, L. R. Cardon, M. S. Phillips, and P. Donnelly, “The effects of human population structure on large genetic association studies,” Nature Genetics, vol. 36, no. 5, pp. 512–517, 2004.
[32]  A. L. Price, N. J. Patterson, R. M. Plenge, M. E. Weinblatt, N. A. Shadick, and D. Reich, “Principal components analysis corrects for stratification in genome-wide association studies,” Nature Genetics, vol. 38, no. 8, pp. 904–909, 2006.
[33]  C. Y. Cheng, D. Reich, J. Coresh et al., “Admixture mapping of obesity-related traits in african americans: the atherosclerosis risk in communities (ARIC) study,” Obesity, vol. 18, no. 3, pp. 563–572, 2010.
[34]  M. H. Park, C. Falconer, R. M. Viner, and S. Kinra, “The impact of childhood obesity on morbidity and mortality in adulthood: a systematic review,” Obesity Reviews, vol. 13, no. 11, pp. 985–1000, 2012.
[35]  A. M. Prentice and S. A. Jebb, “Beyond body mass index,” Obesity Reviews, vol. 2, no. 3, pp. 141–147, 2001.
[36]  P. Deurenberg, M. Yap, and W. A. Van Staveren, “Body mass index and percent body fat: a meta analysis among different ethnic groups,” International Journal of Obesity, vol. 22, no. 12, pp. 1164–1171, 1998.
[37]  K. A. Meyer, E. W. Demerath, S. Friend, P. J. Hannan, and D. Neumark-Sztainer, “Body fat is differentially related to body mass index in U.S.-born African-American and East African immigrant girls,” American Journal of Human Biology, vol. 23, no. 5, pp. 720–723, 2011.
[38]  D. A. Boggs, L. Rosenberg, Y. C. Cozier et al., “General and abdominal obesity and risk of death among black women,” The New England Journal of Medicine, vol. 365, no. 10, pp. 901–908, 2011.
[39]  T. M. Frayling, N. J. Timpson, M. N. Weedon et al., “A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity,” Science, vol. 316, no. 5826, pp. 889–894, 2007.
[40]  J. E. Cecil, R. Tavendale, P. Watt, M. M. Hetherington, and C. N. A. Palmer, “An obesity-associated FTO gene variant and increased energy intake in children,” New England Journal of Medicine, vol. 359, no. 24, pp. 2558–2566, 2008.
[41]  C. S. Fox, Y. Liu, C. C. White et al., et al., “Genome-wide association for abdominal subcutaneous and visceral adipose reveals a novel locus for visceral fat in women,” PLoS Genetics, vol. 8, no. 5, Article ID e1002695, 2012.
[42]  J. Yang, R. J. Loos, J. E. Powell et al., et al., “FTO genotype is associated with phenotypic variability of body mass index,” Nature, vol. 490, no. 7419, pp. 267–272, 2012.
[43]  A. Li and D. Meyre, “Challenges in reproducibility of genetic association studies: lessons learned from the obesity field,” International Journal of Obesity, 2012.
[44]  J. Bressler, W. H. Kao, J. S. Pankow, and E. Boerwinkle, “Risk of type 2 diabetes and obesity is differentially associated with variation in FTO in whites and African-Americans in the ARIC study,” PLoS ONE, vol. 5, no. 5, Article ID e10521, 2010.
[45]  S. D. Rees, M. Islam, M. Z. I. Hydrie et al., “An FTO variant is associated with Type2 diabetes in South Asian populations after accounting for body mass index and waist circumference,” Diabetic Medicine, vol. 28, no. 6, pp. 673–680, 2011.
[46]  F. Ji, M. S. Sharpley, O. Derbeneva et al., et al., “Mitochondrial DNA variant associated with Leber hereditary optic neuropathy and high-altitude Tibetans,” Proceedings of the National Academy of Sciences of the United States of America, vol. 109, no. 19, pp. 7391–7396, 2012.
[47]  R. J. Loos, C. M. Lindgren, S. Li et al., et al., “Common variants near MC4R are associated with fat mass, weight and risk of obesity,” Nature Genetics, vol. 40, no. 6, pp. 768–775, 2008.
[48]  R. Hardy, A. K. Wills, A. Wong et al., “Life course variations in the associations between FTO and MC4R gene variants and body size,” Human Molecular Genetics, vol. 19, no. 3, Article ID ddp504, pp. 545–552, 2009.
[49]  I. S. Farooqi, J. M. Keogh, G. S. H. Yeo, E. J. Lank, T. Cheetham, and S. O'Rahilly, “Clinical spectrum of obesity and mutations in the melanocortin 4 receptor gene,” New England Journal of Medicine, vol. 348, no. 12, pp. 1085–1095, 2003.
[50]  M. D. Fesinmeyer, K. E. North, M. D. Ritchie et al., et al., “Genetic risk factors for BMI and obesity in an ethnically diverse population: results from the population architecture using genomics and epidemiology (PAGE) study,” Obesity, 2012.
[51]  S. F. A. Grant, J. P. Bradfield, H. Zhang et al., “Investigation of the locus near MC4R with childhood obesity in Americans of European and African ancestry,” Obesity, vol. 17, no. 7, pp. 1461–1465, 2009.
[52]  S. J. Kang, C. W. Chiang, C. D. Palmer et al., “Genome-wide association of anthropometric traits in African- and African-derived populations,” Human Molecular Genetics, vol. 19, no. 13, Article ID ddq154, pp. 2725–2738, 2010.
[53]  G. Liu, H. Zhu, V. Lagou et al., “Common variants near melanocortin 4 receptor are associated with general and visceral adiposity in European- and African-American youth,” Journal of Pediatrics, vol. 156, no. 4, pp. 598–605, 2010.
[54]  C. J. Willer, E. K. Speliotes, R. J. Loos et al., et al., “Six new loci associated with body mass index highlight a neuronal influence on body weight regulation,” Nature Genetics, vol. 41, no. 1, pp. 25–34, 2009.
[55]  M. Sch?fer, A. U. Br?uer, N. E. Savaskan, F. G. Rathjen, and T. Brümmendorf, “Neurotractin/kilon promotes neurite outgrowth and is expressed on reactive astrocytes after entorhinal cortex lesion,” Molecular and Cellular Neuroscience, vol. 29, no. 4, pp. 580–590, 2005.
[56]  E. G. Bochukova, N. Huang, J. Keogh et al., “Large, rare chromosomal deletions associated with severe early-onset obesity,” Nature, vol. 463, no. 7281, pp. 666–670, 2010.
[57]  J. Jurvansuu, Y. Zhao, D. S. Y. Leung et al., “Transmembrane protein 18 enhances the tropism of neural stem cells for glioma cells,” Cancer Research, vol. 68, no. 12, pp. 4614–4622, 2008.
[58]  Y. Zhang, R. Proenca, M. Maffei, M. Barone, L. Leopold, and J. M. Friedman, “Positional cloning of the mouse obese gene and its human homologue,” Nature, vol. 372, no. 6505, pp. 425–432, 1994.
[59]  M. C. Ng, J. M. Hester, M. R. Wing et al., “Genome-wide association of BMI in African Americans,” Obesity, vol. 20, no. 3, pp. 622–627, 2012.
[60]  W. Zhao, N. E. Wineinger, H. K. Tiwari et al., “Copy number variations associated with obesity-related traits in African Americans: a joint analysis between GENOA and HyperGEN,” Obesity, vol. 20, no. 12, pp. 2431–2437, 2012.
[61]  C. Q. Lai, K. L. Tucker, S. Choudhry et al., “Population admixture associated with disease prevalence in the Boston Puerto Rican health study,” Human Genetics, vol. 125, no. 2, pp. 199–209, 2009.
[62]  American Diabetes Association, “Diagnosis and classification of diabetes mellitus,” Diabetes Care, vol. 35, supplement 1, pp. S64–S71, 2012.
[63]  W. H. Herman, Y. Ma, G. Uwaifo et al., “Differences in A1C by race and ethnicity among patients with impaired glucose tolerance in the diabetes prevention program,” Diabetes Care, vol. 30, no. 10, pp. 2453–2457, 2007.
[64]  N. M. Maruthur, W. H. Kao, J. M. Clark et al., “Does genetic ancestry explain higher values of glycated hemoglobin in African Americans?” Diabetes, vol. 60, no. 9, pp. 2434–2438, 2011.
[65]  J. K. Bower, F. L. Brancati, and E. Selvin, “No ethnic differences in the association of glycated hemoglobin with retinopathy: the national health and nutrition examination survey 2005–2008,” Diabetes Care, 2012.
[66]  S. Dagogo-Jack, “Pitfalls in the use of HbA 1c as a diagnostic test: the ethnic conundrum,” Nature Reviews Endocrinology, vol. 6, no. 10, pp. 589–593, 2010.
[67]  J. L. Grimsby, B. C. Porneala, J. L. Vassy et al., et al., “Race-ethnic differences in the association of genetic loci with HbA1c levels and mortality in U.S. adults: the third national health and nutrition examination survey (NHANES III),” BMC Medical Genetics, vol. 13, no. 1, article 30, 2012.
[68]  S. Dagogo-Jack, “Predicting diabetes: our relentless quest for genomic nuggets,” Diabetes Care, vol. 35, no. 2, pp. 193–195, 2012.
[69]  S. Dagogo-Jack, “Comment on: Maruthur et al. does genetic ancestry explain higher values of glycated hemoglobin in African Americans? Diabetes 2011, 60: 2434–2438,” Diabetes, vol. 61, no. 1, article e1, 2012.
[70]  S. F. A. Grant, G. Thorleifsson, I. Reynisdottir et al., “Variant of transcription factor 7-like 2 (TCF7L2) gene confers risk of type 2 diabetes,” Nature Genetics, vol. 38, no. 3, pp. 320–323, 2006.
[71]  F. Yi, P. L. Brubaker, and T. Jin, “TCF-4 mediates cell type-specific regulation of proglucagon gene expression by β-catenin and glycogen synthase kinase-3β,” Journal of Biological Chemistry, vol. 280, no. 2, pp. 1457–1464, 2005.
[72]  S. E. Humphries, D. Gable, J. A. Cooper et al., “Common variants in the TCF7L2 gene and predisposition to type 2 diabetes in UK European Whites, Indian Asians and Afro-Caribbean men and women,” Journal of Molecular Medicine, vol. 84, no. 12, pp. 1005–1014, 2006.
[73]  J. C. Florez, K. A. Jablonski, N. Bayley et al., “TCF7L2 polymorphisms and progression to diabetes in the Diabetes Prevention Program,” New England Journal of Medicine, vol. 355, no. 3, pp. 241–250, 2006.
[74]  M. M. Sale, S. G. Smith, J. C. Mychaleckyj et al., “Variants of the transcription factor 7-like 2 (TCF7L2) gene are associated with type 2 diabetes in an African-American population enriched for nephropathy,” Diabetes, vol. 56, no. 10, pp. 2638–2642, 2007.
[75]  J. P. Lewis, N. D. Palmer, P. J. Hicks et al., “Association analysis in African Americans of European-derived type 2 diabetes single nucleotide polymorphisms from whole-genome association studies,” Diabetes, vol. 57, no. 8, pp. 2220–2225, 2008.
[76]  D. Dabelea, L. M. Dolan, R. D'Agostino et al., “Association testing of TCF7L2 polymorphisms with type 2 diabetes in multi-ethnic youth,” Diabetologia, vol. 54, no. 3, pp. 535–539, 2011.
[77]  Y. Yan, K. E. North, C. M. Ballantyne et al., “Transcription factor 7-like 2 (TCF7L2) polymorphism and context-specific risk of type 2 diabetes in African American and caucasian adults: the atherosclerosis risk in communities study,” Diabetes, vol. 58, no. 1, pp. 285–289, 2009.
[78]  S. Cauchi, Y. El Achhab, H. Choquet et al., “TCF7L2 is reproducibly associated with type 2 diabetes in various ethnic groups: a global meta-analysis,” Journal of Molecular Medicine, vol. 85, no. 7, pp. 777–782, 2007.
[79]  A. Helgason, S. Pálsson, G. Thorleifsson et al., “Refining the impact of TCF7L2 gene variants on type 2 diabetes and adaptive evolution,” Nature Genetics, vol. 39, no. 2, pp. 218–225, 2007.
[80]  J. B. Maller, G. McVean, J. Byrnes et al., “Bayesian refinement of association signals for 14 loci in 3 common diseases,” Nature Genetics, vol. 44, no. 12, pp. 1294–1301, 2012.
[81]  J. Munoz, K. H. Lok, B. A. Gower et al., “Polymorphism in the transcription factor 7-like 2 (TCF7L2) gene is associated with reduced insulin secretion in nondiabetic women,” Diabetes, vol. 55, no. 12, pp. 3630–3634, 2006.
[82]  N. D. Palmer, A. B. Lehtinen, C. D. Langefeld et al., “Association of TCF7L2 gene polymorphisms with reduced acute insulin response in Hispanic Americans,” Journal of Clinical Endocrinology and Metabolism, vol. 93, no. 1, pp. 304–309, 2008.
[83]  S. C. Elbein, W. S. Chu, S. K. Das et al., “Transcription factor 7-like 2 polymorphisms and type 2 diabetes, glucose homeostasis traits and gene expression in US participants of European and African descent,” Diabetologia, vol. 50, no. 8, pp. 1621–1630, 2007.
[84]  K. M. Waters, D. O. Stram, M. T. Hassanein et al., “Consistent association of type 2 diabetes risk variants found in europeans in diverse racial and ethnic groups,” PLoS Genetics, vol. 6, no. 8, 2010.
[85]  C. A. Haiman, M. D. Fesinmeyer, K. L. Spencer et al., et al., “Consistent directions of effect for established type 2 diabetes risk variants across populations: the population architecture using Genomics and Epidemiology (PAGE) Consortium,” Diabetes, vol. 61, no. 6, pp. 1642–1647, 2012.
[86]  J. N. Cooke, M. C. Ng, N. D. Palmer et al., “Genetic risk assessment of type 2 diabetes-associated polymorphisms in African Americans,” Diabetes Care, vol. 35, no. 2, pp. 287–292, 2012.
[87]  K. A. Langberg, L. Ma, N. K. Sharma et al., et al., “Single nucleotide polymorphisms in JAZF1 and BCL11A gene are nominally associated with type 2 diabetes in African-American families from the GENNID study,” Journal of Human Genetics, vol. 57, no. 1, pp. 57–61, 2012.
[88]  P. Liu, J. R. Keller, M. Ortiz et al., “Bcl11a is essential for normal lymphoid development,” Nature Immunology, vol. 4, no. 6, pp. 525–532, 2003.
[89]  H. Li, J. Wang, G. Mor, and J. Sklar, “A neoplastic gene fusion mimics trans-splicing of RNAs in normal human cells,” Science, vol. 321, no. 5894, pp. 1357–1361, 2008.
[90]  T. M. Strom, K. H?rtnagel, S. Hofmann et al., “Diabetes insipidus, diabetes mellitus, optic atrophy and deafness (DIDMOAD) caused by mutations in a novel gene (wolframin) coding for a predicted transmembrane protein,” Human Molecular Genetics, vol. 7, no. 13, pp. 2021–2028, 1998.
[91]  N. D. Palmer, M. O. Goodarzi, C. D. Langefeld et al., “Quantitative trait analysis of type 2 diabetes susceptibility loci identified from whole genome association studies in the insulin resistance atherosclerosis family study,” Diabetes, vol. 57, no. 4, pp. 1093–1100, 2008.
[92]  N. D. Palmer, C. W. McDonough, P. J. Hicks et al., et al., “A genome-wide association search for type 2 diabetes genes in African Americans,” PLoS ONE, vol. 7, no. 1, Article ID e29202, 2012.
[93]  G. Chen, A. Bentley, A. Adeyemo et al., “Genome-wide association study identifies novel loci association with fasting insulin and insulin resistance in African Americans,” Human Molecular Genetics, vol. 21, no. 20, pp. 4530–4536, 2012.
[94]  R. Chen, E. Corona, M. Sikora et al., “Type 2 diabetes risk alleles demonstrate extreme directional differentiation among human populations, compared to other diseases,” PLoS Genetics, vol. 8, no. 4, Article ID e1002621, 2012.
[95]  G. Genovese, D. J. Friedman, M. D. Ross et al., “Association of trypanolytic ApoL1 variants with kidney disease in African Americans,” Science, vol. 329, no. 5993, pp. 841–845, 2010.
[96]  C. Wilson, “Health policy: endocrine health for all-finding and eliminating health disparities in endocrine disorders,” Nature Reviews Endocrinology, vol. 8, no. 9, p. 503, 2012.
[97]  N. D. Palmer, J. M. Hester, S. S. An et al., “Resequencing and analysis of variation in the TCF7L2 gene in African Americans suggests that SNP rs7903146 is the causal diabetes susceptibility variant,” Diabetes, vol. 60, no. 2, pp. 662–668, 2011.

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