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Article ; Online: Epigenome-wide association study of plasma lipids in West Africans

Eva L. van der Linden / Karlijn A.C. Meeks / Felix Chilunga / Charles Hayfron-Benjamin / Silver Bahendeka / Kerstin Klipstein-Grobusch / Andrea Venema / Bert-Jan van den Born / Charles Agyemang / Peter Henneman / Adebowale Adeyemo

EBioMedicine, Vol 89, Iss , Pp 104469- (2023)

the RODAM studyResearch in context

2023

Abstract: Summary: Background: DNA-methylation has been associated with plasma lipid concentration in populations of diverse ethnic backgrounds, but epigenome-wide association studies (EWAS) in West-Africans are lacking. The aim of this study was to identify DNA- ... ...

Abstract	Summary: Background: DNA-methylation has been associated with plasma lipid concentration in populations of diverse ethnic backgrounds, but epigenome-wide association studies (EWAS) in West-Africans are lacking. The aim of this study was to identify DNA-methylation loci associated with plasma lipids in Ghanaians. Methods: We conducted an EWAS using Illumina 450k DNA-methylation array profiles of extracted DNA from 663 Ghanaian participants. Differentially methylated positions (DMPs) were examined for association with plasma total cholesterol (TC), LDL-cholesterol, HDL-cholesterol, and triglycerides concentrations using linear regression models adjusted for age, sex, body mass index, diabetes mellitus, and technical covariates. Findings were replicated in independent cohorts of different ethnicities. Findings: We identified one significantly associated DMP with triglycerides (cg19693031 annotated to TXNIP, regression coefficient beta −0.26, false discovery rate adjusted p-value 0.001), which replicated in-silico in South African Batswana, African American, and European populations. From the top five DMPs with the lowest nominal p-values, two additional DMPs for triglycerides (CPT1A, ABCG1), two DMPs for LDL-cholesterol (EPSTI1, cg13781819), and one for TC (TXNIP) replicated. With the exception of EPSTI1, these loci are involved in lipid transport/metabolism or are known GWAS-associated loci. The top 5 DMPs per lipid trait explained 9.5% in the variance of TC, 8.3% in LDL-cholesterol, 6.1% in HDL-cholesterol, and 11.0% in triglycerides. Interpretation: The top DMPs identified in this study are in loci that play a role in lipid metabolism across populations, including West-Africans. Future studies including larger sample size, longitudinal study design and translational research is needed to increase our understanding on the epigenetic regulation of lipid metabolism among West-African populations. Funding: European Commission under the Framework Programme (grant number: 278901).
Keywords	Methylation ; Epigenome-wide association study ; Cholesterol ; Lipids ; Sub-Saharan Africa ; West Africa ; Medicine ; R ; Medicine (General) ; R5-920
Subject code	310
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A UGT1A1 variant is associated with serum total bilirubin levels, which are causal for hypertension in African-ancestry individuals

Guanjie Chen / Adebowale Adeyemo / Jie Zhou / Ayo P. Doumatey / Amy R. Bentley / Kenneth Ekoru / Daniel Shriner / Charles N. Rotimi

npj Genomic Medicine, Vol 6, Iss 1, Pp 1-

2021 Volume 6

Abstract: Abstract Serum bilirubin is associated with several clinical outcomes, including hypertension, type 2 diabetes (T2D), and drug metabolism. Here, we describe findings from our genome-wide association studies (GWAS) of serum (TBIL) using a generalized ... ...

Abstract	Abstract Serum bilirubin is associated with several clinical outcomes, including hypertension, type 2 diabetes (T2D), and drug metabolism. Here, we describe findings from our genome-wide association studies (GWAS) of serum (TBIL) using a generalized linear mixed model in West Africans (n = 1127), with adjustment for age, sex, body mass index, T2D, significant principal components of population structure, and cryptic relatedness. Genome-wide conditional analysis and CAVIARBF were used to fine map significant loci. The causal effect of TBIL on hypertension was assessed by Mendelian randomization (MR) using the GWAS findings as instrumental variables (IVs) in African Americans (n = 3,067). The SNP rs887829 (UGT1A1) was significantly associated with TBIL levels (effect allele (T) frequency = 0.49, β (SE) = 0.59 (0.04), p = 9.13 × 10−54). Genome-wide conditional analysis and regional fine mapping pointed to rs887829 as a possible causal variant with a posterior inclusion probability of 0.99. The T allele of rs887829 is associated with lower hepatic expression of UGT1A1. Using rs887829 as an IV, two-stage least-squares MR showed a causal effect of bilirubin on hypertension (β = −0.76, 95% CI [−1.52, −0.01], p = 0.0459). Our finding confirms that UGT1A1 influences bilirubin levels. Notably, lower TBIL is causally associated with the increased risk of hypertension.
Keywords	Medicine ; R ; Genetics ; QH426-470
Subject code	616
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Additive genetic effect of GCKR, G6PC2, and SLC30A8 variants on fasting glucose levels and risk of type 2 diabetes.

Guanjie Chen / Daniel Shriner / Jianhua Zhang / Jie Zhou / Poorni Adikaram / Ayo P Doumatey / Amy R Bentley / Adebowale Adeyemo / Charles N Rotimi

PLoS ONE, Vol 17, Iss 6, p e

2022 Volume 0269378

Abstract: Impaired glucose tolerance is a major risk factor for type 2 diabetes (T2D) and several cardiometabolic disorders. To identify genetic loci underlying fasting glucose levels, we conducted an analysis of 9,232 individuals of European ancestry who at ... ...

Abstract	Impaired glucose tolerance is a major risk factor for type 2 diabetes (T2D) and several cardiometabolic disorders. To identify genetic loci underlying fasting glucose levels, we conducted an analysis of 9,232 individuals of European ancestry who at enrollment were either nondiabetic or had untreated type 2 diabetes. Multivariable linear mixed models were used to test for associations between fasting glucose and 7.9 million SNPs, with adjustment for age, body mass index (BMI), sex, significant principal components of the genotypes, and cryptic relatedness. Three previously discovered loci were genome-wide significant, with the lead SNPs being rs1260326, a missense variant in GCKR (p = 1.06×10-8); rs560887, an intronic variant in G6PC2 (p = 3.39×10-11); and rs13266634, a missense variant in SLC30A8 (p = 4.28×10-10). Fine mapping, genome-wide conditional analysis, and functional annotation indicated that the three loci were independently associated with fasting glucose. Each copy of an alternate allele at any of these three SNPs was associated with a reduction of 0.012 mmol/L in fasting glucose levels (p = 8.0×10-28), and this association was replicated in trans-ethnic analysis of 14,303 individuals (p = 2.2×10-16). The three SNPs were jointly associated with significantly reduced T2D risk, with an odds ratio (95% CI) of 0.93 (0.88, 0.98) per protective allele. Our findings implicate additive effects across pathophysiological pathways involved in type 2 diabetes, including glycolysis, gluconeogenesis, and insulin secretion. Since none of the individuals homozygous for the alternate alleles at all three loci has T2D, it might be possible to use a genetic predictor of fasting glucose levels to identify individuals at low vs. high risk of developing type 2 diabetes.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Additive genetic effect of GCKR, G6PC2, and SLC30A8 variants on fasting glucose levels and risk of type 2 diabetes

Guanjie Chen / Daniel Shriner / Jianhua Zhang / Jie Zhou / Poorni Adikaram / Ayo P. Doumatey / Amy R. Bentley / Adebowale Adeyemo / Charles N. Rotimi

PLoS ONE, Vol 17, Iss

2022 Volume 6

Abstract	Impaired glucose tolerance is a major risk factor for type 2 diabetes (T2D) and several cardiometabolic disorders. To identify genetic loci underlying fasting glucose levels, we conducted an analysis of 9,232 individuals of European ancestry who at enrollment were either nondiabetic or had untreated type 2 diabetes. Multivariable linear mixed models were used to test for associations between fasting glucose and 7.9 million SNPs, with adjustment for age, body mass index (BMI), sex, significant principal components of the genotypes, and cryptic relatedness. Three previously discovered loci were genome-wide significant, with the lead SNPs being rs1260326, a missense variant in GCKR (p = 1.06×10−8); rs560887, an intronic variant in G6PC2 (p = 3.39×10−11); and rs13266634, a missense variant in SLC30A8 (p = 4.28×10−10). Fine mapping, genome-wide conditional analysis, and functional annotation indicated that the three loci were independently associated with fasting glucose. Each copy of an alternate allele at any of these three SNPs was associated with a reduction of 0.012 mmol/L in fasting glucose levels (p = 8.0×10−28), and this association was replicated in trans-ethnic analysis of 14,303 individuals (p = 2.2×10−16). The three SNPs were jointly associated with significantly reduced T2D risk, with an odds ratio (95% CI) of 0.93 (0.88, 0.98) per protective allele. Our findings implicate additive effects across pathophysiological pathways involved in type 2 diabetes, including glycolysis, gluconeogenesis, and insulin secretion. Since none of the individuals homozygous for the alternate alleles at all three loci has T2D, it might be possible to use a genetic predictor of fasting glucose levels to identify individuals at low vs. high risk of developing type 2 diabetes.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Time-to-event modeling of hypertension reveals the nonexistence of true controls

Daniel Shriner / Amy R Bentley / Jie Zhou / Kenneth Ekoru / Ayo P Doumatey / Guanjie Chen / Adebowale Adeyemo / Charles N Rotimi

eLife, Vol

2020 Volume 9

Abstract: Given a lifetime risk of ~90% by the ninth decade of life, it is unknown if there are true controls for hypertension in epidemiological and genetic studies. Here, we compared Bayesian logistic and time-to-event approaches to modeling hypertension. The ... ...

Abstract	Given a lifetime risk of ~90% by the ninth decade of life, it is unknown if there are true controls for hypertension in epidemiological and genetic studies. Here, we compared Bayesian logistic and time-to-event approaches to modeling hypertension. The median age at hypertension was approximately a decade earlier in African Americans than in European Americans or Mexican Americans. The probability of being free of hypertension at 85 years of age in African Americans was less than half that in European Americans or Mexican Americans. In all groups, baseline hazard rates increased until nearly 60 years of age and then decreased but did not reach zero. Taken together, modeling of the baseline hazard function of hypertension suggests that there are no true controls and that controls in logistic regression are cases with a late age of onset.
Keywords	hypertension ; time-to-event ; health disparity ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2020-12-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Genome-wide association study for proliferative diabetic retinopathy in Africans

Chang Liu / Guanjie Chen / Amy R. Bentley / Ayo Doumatey / Jie Zhou / Adebowale Adeyemo / Jinkui Yang / Charles Rotimi

npj Genomic Medicine, Vol 4, Iss 1, Pp 1-

2019 Volume 7

Abstract: Abstract Proliferative diabetic retinopathy (PDR) is a sight-threatening complication of diabetes that is associated with longer duration of diabetes and poor glycemic control under a genetic susceptibility background. Although GWAS of PDR have been ... ...

Abstract	Abstract Proliferative diabetic retinopathy (PDR) is a sight-threatening complication of diabetes that is associated with longer duration of diabetes and poor glycemic control under a genetic susceptibility background. Although GWAS of PDR have been conducted in Europeans and Asians, none has been done in continental Africans, a population at increased risk for PDR. Here, we report a GWAS of PDR among Africans. PDR cases (n = 64) were T2D patients with neovascularization in the retina and/or retinal detachment. Controls (n = 227) were T2D patients without listed eye complications despite high risk (T2D duration ≥10 years and fasting blood glucose >169 mg/dl). Replication was assessed in African Americans enrolled in the ARIC study. We identified 4 significant loci: WDR72, HLA-B, GAP43/RP11-326J18.1, and AL713866.1. At WDR72 the most strongly associated SNPs were rs12906891 (MAF = 0.071; p = 9.68 × 10-10; OR = 1.46, 95% CI [1.30,1.64]) and rs11070992 (MAF = 0.14; p = 4.23 × 10−8; OR = 1.28, 95%CI [1.17–1.40]). rs11070992 replicated in African Americans (p = 0.04). Variants in this gene have been associated with diabetic retinopathy, glycemic control, revascularization, and kidney disease.
Keywords	Medicine ; R ; Genetics ; QH426-470
Language	English
Publishing date	2019-08-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Circulating MiR-374a-5p is a potential modulator of the inflammatory process in obesity

Ayo P. Doumatey / William J. He / Amadou Gaye / Lin Lei / Jie Zhou / Gary H. Gibbons / Adebowale Adeyemo / Charles N. Rotimi

Scientific Reports, Vol 8, Iss 1, Pp 1-

2018 Volume 9

Abstract: Abstract Obese individuals without expected metabolic co-morbidities are referred to as metabolically healthy obese (MHO). The molecular mechanisms underlying this phenotype remain elusive. MicroRNAs may be involved in the MHO phenotype. To test this ... ...

Abstract	Abstract Obese individuals without expected metabolic co-morbidities are referred to as metabolically healthy obese (MHO). The molecular mechanisms underlying this phenotype remain elusive. MicroRNAs may be involved in the MHO phenotype. To test this hypothesis, we screened 179 serum miRNAs in 20 African-American women (10 MHOs and 10 metabolically abnormal obese individuals -MAO). We identified 8 differentially expressed miRNAs (DEMs) with validation in an independent sample of 64 MHO and 34 MAO. Of the eight DEMs in the screening phase (p ≤ 0.05), miR-374a-5p remained significant (p = 0.04) with directional consistency in the validation sample. Ingenuity Pathway analysis revealed that miR-374a-5p putatively targeted 37 mRNAs (e.g. chemokines and transcription factors) which are members of canonical pathways involved in inflammation (IL-17A signaling) and lipid metabolism. Analysis restricted to adipocytes, the main source of circulating miRNAs in obesity, identified 3 mRNAs (CCL2, STEAP2, EN1) as the main target of miR-374a-5p. Evaluation of the 3 mRNAs in an independent sample showed that CCL2 was significantly downregulated (p = 0.0005). In summary, MiR-374a-5p is upregulated in MHO compared to MAO individuals and appears to show association with downregulation of pro-inflammatory markers that are linked to insulin resistance. Given the correlative nature of our findings, functional studies are needed.
Keywords	Medicine ; R ; Science ; Q
Subject code	571
Language	English
Publishing date	2018-05-01T00:00:00Z
Publisher	Nature Publishing Group
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Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Joint ancestry and association testing in admixed individuals.

Daniel Shriner / Adebowale Adeyemo / Charles N Rotimi

PLoS Computational Biology, Vol 7, Iss 12, p e

2011 Volume 1002325

Abstract: For samples of admixed individuals, it is possible to test for both ancestry effects via admixture mapping and genotype effects via association mapping. Here, we describe a joint test called BMIX that combines admixture and association statistics at ... ...

Abstract	For samples of admixed individuals, it is possible to test for both ancestry effects via admixture mapping and genotype effects via association mapping. Here, we describe a joint test called BMIX that combines admixture and association statistics at single markers. We first perform high-density admixture mapping using local ancestry. We then perform association mapping using stratified regression, wherein for each marker genotypes are stratified by local ancestry. In both stages, we use generalized linear models, providing the advantage that the joint test can be used with any phenotype distribution with an appropriate link function. To define the alternative densities for admixture mapping and association mapping, we describe a method based on autocorrelation to empirically estimate the testing burdens of admixture mapping and association mapping. We then describe a joint test that uses the posterior probabilities from admixture mapping as prior probabilities for association mapping, capitalizing on the reduced testing burden of admixture mapping relative to association mapping. By simulation, we show that BMIX is potentially orders-of-magnitude more powerful than the MIX score, which is currently the most powerful frequentist joint test. We illustrate the gain in power through analysis of fasting plasma glucose among 922 unrelated, non-diabetic, admixed African Americans from the Howard University Family Study. We detected loci at 1q24 and 6q26 as genome-wide significant via admixture mapping; both loci have been independently reported from linkage analysis. Using the association data, we resolved the 1q24 signal into two regions. One region, upstream of the gene FAM78B, contains three binding sites for the transcription factor PPARG and two binding sites for HNF1A, both previously implicated in the pathology of type 2 diabetes. The fact that both loci showed ancestry effects may provide novel insight into the genetic architecture of fasting plasma glucose in individuals of African ancestry.
Keywords	Biology (General) ; QH301-705.5
Subject code	401
Language	English
Publishing date	2011-12-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
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Article ; Online: Genetic modifiers of long‐term survival in sickle cell anemia

Ambroise Wonkam / Emile R. Chimusa / Khuthala Mnika / Gift Dineo Pule / Valentina Josiane Ngo Bitoungui / Nicola Mulder / Daniel Shriner / Charles N. Rotimi / Adebowale Adeyemo

Clinical and Translational Medicine, Vol 10, Iss 4, Pp n/a-n/a (2020)

2020

Abstract: Abstract Background Sickle cell anemia (SCA) is a clinically heterogeneous, monogenic disorder. Medical care has less‐than‐optimal impact on clinical outcomes in SCA in Africa due to several factors, including patient accessibility, poor access to ... ...

Abstract	Abstract Background Sickle cell anemia (SCA) is a clinically heterogeneous, monogenic disorder. Medical care has less‐than‐optimal impact on clinical outcomes in SCA in Africa due to several factors, including patient accessibility, poor access to resources, and non‐availability of specific effective interventions for SCA. Methods Against this background, we investigated 192 African participants who underwent whole exome sequencing. Participants included 105 SCA patients spanning variable clinical expression: a “long survivor” group (age over 40 years), a “stroke” group (at least one episode of overt stroke), and a “random” group (patients younger than 40 years without overt cerebrovascular disease). Fifty‐eight ethnically matched homozygous hemoglobin A controls were also studied. Findings were validated in an independently recruited sample of 29 SCA patients. Statistical significance of the mutational burden of deleterious and loss‐of‐function variants per gene against a null model was estimated for each group, and gene‐set association tests were conducted to test differences between groups. Results In the “long survivor” group, deleterious/loss‐of‐function variants were enriched in genes including CLCN6 (a voltage‐dependent chloride channel for which rare deleterious variants have been associated with lower blood pressure) and OGHDL (important in arginine metabolism, which is a therapeutic target in SCA). In the “stroke” group, significant genes implicated were associated with increased activity of the blood coagulation cascade and increased complement activation, for example, SERPINC1, which encodes antithrombin. Oxidative stress and glutamate biosynthesis pathways were enriched in “long survivors” group. Published transcriptomic evidence provides functional support for the role of the identified pathways. Conclusions This study provides new gene sets that contribute to variability in clinical expression of SCA. Identified genes and pathways suggest new avenues for other interventions.
Keywords	Africa ; genetic modifiers ; sickle cell disease ; whole exome sequencing ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2020-08-01T00:00:00Z
Publisher	Wiley
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Article ; Online: Genome-wide DNA methylation analysis on C-reactive protein among Ghanaians suggests molecular links to the emerging risk of cardiovascular diseases

Felix P. Chilunga / Peter Henneman / Andrea Venema / Karlijn A. C. Meeks / Ana Requena-Méndez / Erik Beune / Frank P. Mockenhaupt / Liam Smeeth / Silver Bahendeka / Ina Danquah / Kerstin Klipstein-Grobusch / Adebowale Adeyemo / Marcel M.A.M Mannens / Charles Agyemang

npj Genomic Medicine, Vol 6, Iss 1, Pp 1-

2021 Volume 9

Abstract: Abstract Molecular mechanisms at the intersection of inflammation and cardiovascular diseases (CVD) among Africans are still unknown. We performed an epigenome-wide association study to identify loci associated with serum C-reactive protein (marker of ... ...

Abstract	Abstract Molecular mechanisms at the intersection of inflammation and cardiovascular diseases (CVD) among Africans are still unknown. We performed an epigenome-wide association study to identify loci associated with serum C-reactive protein (marker of inflammation) among Ghanaians and further assessed whether differentially methylated positions (DMPs) were linked to CVD in previous reports, or to estimated CVD risk in the same population. We used the Illumina Infinium® HumanMethylation450 BeadChip to obtain DNAm profiles of blood samples in 589 Ghanaians from the RODAM study (without acute infections, not taking anti-inflammatory medications, CRP levels < 40 mg/L). We then used linear models to identify DMPs associated with CRP concentrations. Post-hoc, we evaluated associations of identified DMPs with elevated CVD risk estimated via ASCVD risk score. We also performed subset analyses at CRP levels ≤10 mg/L and replication analyses on candidate probes. Finally, we assessed for biological relevance of our findings in public databases. We subsequently identified 14 novel DMPs associated with CRP. In post-hoc evaluations, we found that DMPs in PC, BTG4 and PADI1 showed trends of associations with estimated CVD risk, we identified a separate DMP in MORC2 that was associated with CRP levels ≤10 mg/L, and we successfully replicated 65 (24%) of previously reported DMPs. All DMPs with gene annotations (13) were biologically linked to inflammation or CVD traits. We have identified epigenetic loci that may play a role in the intersection between inflammation and CVD among Ghanaians. Further studies among other Africans are needed to confirm our findings.
Keywords	Medicine ; R ; Genetics ; QH426-470
Subject code	610
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	Nature Portfolio
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