A Copy Number Variant on Chromosome 20q13.3 Implicated in Thinness and Severe Obesity

Background/Objectives. To identify copy number variants (CNVs) which are associated with body mass index (BMI). Subjects/Methods. CNVs were identified using array comparative genomic hybridization (aCGH) on members of pedigrees ascertained through severely obese (BMI ≥ 35 kg/m2) sib pairs (86 pedigr...

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Published inJournal of Obesity Vol. 2015; no. 2015; pp. 246 - 252
Main Authors Adams, Ted D., Lewis, Tracey, Mao, Rong, Xin, Yuanpei, Hasstedt, Sandra J., Hunt, Steven C.
Format Journal Article
LanguageEnglish
Published Cairo, Egypt Hindawi Limiteds 01.01.2015
Hindawi Publishing Corporation
John Wiley & Sons, Inc
Wiley
Subjects
ADP-Ribosylation Factors - genetics
Adult
Aged
Aged, 80 and over
Alleles
Analysis
Body Mass Index
Chromosomes
Chromosomes, Human, Pair 20
Colleges & universities
Comparative Genomic Hybridization
Copy number variations
Deoxyribonucleic acid
DNA
DNA Copy Number Variations
Drug dosages
Families & family life
Female
Genes
Genetic aspects
Genetic Pleiotropy
Genetic Predisposition to Disease
Genetic variation
Genetics
Genome-Wide Association Study
Genomes
Genomics
Genotype
Humans
Male
Medicine
Middle Aged
Obesity
Obesity, Morbid - genetics
Pedigree
Physiological aspects
Reference Values
Risk factors
Sequence Deletion
Software
Thinness - genetics
Young Adult
United States
Qatar
Online AccessGet full text

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Abstract Background/Objectives. To identify copy number variants (CNVs) which are associated with body mass index (BMI). Subjects/Methods. CNVs were identified using array comparative genomic hybridization (aCGH) on members of pedigrees ascertained through severely obese (BMI ≥ 35 kg/m2) sib pairs (86 pedigrees) and thin (BMI ≤ 23 kg/m2) probands (3 pedigrees). Association was inferred through pleiotropy of BMI with CNV log⁡2 intensity ratio. Results. A 77-kilobase CNV on chromosome 20q13.3, confirmed by real-time qPCR, exhibited deletions in the obese subjects and duplications in the thin subjects (P=2.2×10-6). Further support for the presence of a deletion derived from inference by likelihood analysis of null alleles for SNPs residing in the region. Conclusions. One or more of 7 genes residing in a chromosome 20q13.3 CNV region appears to influence BMI. The strongest candidate is ARFRP1, which affects glucose metabolism in mice.
AbstractList [ProQuest: [...] denotes non US-ASCII text; see PDF] Background/Objectives. To identify copy number variants (CNVs) which are associated with body mass index (BMI). Subjects/Methods. CNVs were identified using array comparative genomic hybridization (aCGH) on members of pedigrees ascertained through severely obese (BMI ≥ 35 kg/m2) sib pairs (86 pedigrees) and thin (BMI <= 23 kg/m2) probands (3 pedigrees). Association was inferred through pleiotropy of BMI with CNV log[...]2 intensity ratio. Results. A 77-kilobase CNV on chromosome 20q13.3, confirmed by real-time qPCR, exhibited deletions in the obese subjects and duplications in the thin subjects (P=2.2×[superscript]10-6[/superscript] ). Further support for the presence of a deletion derived from inference by likelihood analysis of null alleles for SNPs residing in the region. Conclusions. One or more of 7 genes residing in a chromosome 20q13.3 CNV region appears to influence BMI. The strongest candidate is ARFRP1, which affects glucose metabolism in mice.
Background/Objectives. To identify copy number variants (CNVs) which are associated with body mass index (BMI). Subjects/Methods. CNVs were identified using array comparative genomic hybridization (aCGH) on members of pedigrees ascertained through severely obese (BMI ≥ 35 kg/m2) sib pairs (86 pedigrees) and thin (BMI ≤ 23 kg/m2) probands (3 pedigrees). Association was inferred through pleiotropy of BMI with CNV log⁡2 intensity ratio. Results. A 77-kilobase CNV on chromosome 20q13.3, confirmed by real-time qPCR, exhibited deletions in the obese subjects and duplications in the thin subjects (P=2.2×10-6). Further support for the presence of a deletion derived from inference by likelihood analysis of null alleles for SNPs residing in the region. Conclusions. One or more of 7 genes residing in a chromosome 20q13.3 CNV region appears to influence BMI. The strongest candidate is ARFRP1, which affects glucose metabolism in mice.
Background/Objectives. To identify copy number variants (CNVs) which are associated with body mass index (BMI). Subjects/Methods. CNVs were identified using array comparative genomic hybridization (aCGH) on members of pedigrees ascertained through severely obese (BMI [greater than or equal to] 35 kg/[m.sup.2]) sib pairs (86 pedigrees) and thin (BMI [less than or equal to] 23 kg/[m.sup.2]) probands (3 pedigrees). Association was inferred through pleiotropy of BMI with CNV log 2 intensity ratio. Results. A 77-kilobase CNV on chromosome 20q13.3, confirmed by real-time qPCR, exhibited deletions in the obese subjects and duplications in the thin subjects (P = 2.2 x [10.sup.-6]). Further support for the presence of a deletion derived from inference by likelihood analysis of null alleles for SNPs residing in the region. Conclusions. One or more of 7 genes residing in a chromosome 20q13.3 CNV region appears to influence BMI. The strongest candidate is ARFRP1, which affects glucose metabolism in mice.
To identify copy number variants (CNVs) which are associated with body mass index (BMI). CNVs were identified using array comparative genomic hybridization (aCGH) on members of pedigrees ascertained through severely obese (BMI ≥ 35 kg/m(2)) sib pairs (86 pedigrees) and thin (BMI ≤ 23 kg/m(2)) probands (3 pedigrees). Association was inferred through pleiotropy of BMI with CNV log⁡2 intensity ratio. A 77-kilobase CNV on chromosome 20q13.3, confirmed by real-time qPCR, exhibited deletions in the obese subjects and duplications in the thin subjects (P = 2.2 × 10(-6)). Further support for the presence of a deletion derived from inference by likelihood analysis of null alleles for SNPs residing in the region. One or more of 7 genes residing in a chromosome 20q13.3 CNV region appears to influence BMI. The strongest candidate is ARFRP1, which affects glucose metabolism in mice.
Background/Objectives. To identify copy number variants (CNVs) which are associated with body mass index (BMI). Subjects/Methods. CNVs were identified using array comparative genomic hybridization (aCGH) on members of pedigrees ascertained through severely obese (BMI ≥ 35 kg/m 2 ) sib pairs (86 pedigrees) and thin (BMI ≤ 23 kg/m 2 ) probands (3 pedigrees). Association was inferred through pleiotropy of BMI with CNV log ⁡ 2 intensity ratio. Results. A 77-kilobase CNV on chromosome 20q13.3, confirmed by real-time qPCR, exhibited deletions in the obese subjects and duplications in the thin subjects ( P = 2.2 × 10 - 6 ). Further support for the presence of a deletion derived from inference by likelihood analysis of null alleles for SNPs residing in the region. Conclusions. One or more of 7 genes residing in a chromosome 20q13.3 CNV region appears to influence BMI. The strongest candidate is ARFRP1 , which affects glucose metabolism in mice.
Background/Objectives. To identify copy number variants (CNVs) which are associated with body mass index (BMI). Subjects/Methods. CNVs were identified using array comparative genomic hybridization (aCGH) on members of pedigrees ascertained through severely obese (BMI ≥ 35 kg/m 2 ) sib pairs (86 pedigrees) and thin (BMI ≤ 23 kg/m 2 ) probands (3 pedigrees). Association was inferred through pleiotropy of BMI with CNV log⁡2 intensity ratio. Results. A 77-kilobase CNV on chromosome 20q13.3, confirmed by real-time qPCR, exhibited deletions in the obese subjects and duplications in the thin subjects ( P = 2.2 × 10 −6 ). Further support for the presence of a deletion derived from inference by likelihood analysis of null alleles for SNPs residing in the region. Conclusions. One or more of 7 genes residing in a chromosome 20q13.3 CNV region appears to influence BMI. The strongest candidate is ARFRP1 , which affects glucose metabolism in mice.
To identify copy number variants (CNVs) which are associated with body mass index (BMI).BACKGROUND/OBJECTIVESTo identify copy number variants (CNVs) which are associated with body mass index (BMI).CNVs were identified using array comparative genomic hybridization (aCGH) on members of pedigrees ascertained through severely obese (BMI ≥ 35 kg/m(2)) sib pairs (86 pedigrees) and thin (BMI ≤ 23 kg/m(2)) probands (3 pedigrees). Association was inferred through pleiotropy of BMI with CNV log⁡2 intensity ratio.SUBJECTS/METHODSCNVs were identified using array comparative genomic hybridization (aCGH) on members of pedigrees ascertained through severely obese (BMI ≥ 35 kg/m(2)) sib pairs (86 pedigrees) and thin (BMI ≤ 23 kg/m(2)) probands (3 pedigrees). Association was inferred through pleiotropy of BMI with CNV log⁡2 intensity ratio.A 77-kilobase CNV on chromosome 20q13.3, confirmed by real-time qPCR, exhibited deletions in the obese subjects and duplications in the thin subjects (P = 2.2 × 10(-6)). Further support for the presence of a deletion derived from inference by likelihood analysis of null alleles for SNPs residing in the region.RESULTSA 77-kilobase CNV on chromosome 20q13.3, confirmed by real-time qPCR, exhibited deletions in the obese subjects and duplications in the thin subjects (P = 2.2 × 10(-6)). Further support for the presence of a deletion derived from inference by likelihood analysis of null alleles for SNPs residing in the region.One or more of 7 genes residing in a chromosome 20q13.3 CNV region appears to influence BMI. The strongest candidate is ARFRP1, which affects glucose metabolism in mice.CONCLUSIONSOne or more of 7 genes residing in a chromosome 20q13.3 CNV region appears to influence BMI. The strongest candidate is ARFRP1, which affects glucose metabolism in mice.
Audience Academic
Author Xin, Yuanpei
Adams, Ted D.
Hasstedt, Sandra J.
Lewis, Tracey
Mao, Rong
Hunt, Steven C.
AuthorAffiliation 1 Department of Human Genetics, University of Utah School of Medicine, Salt Lake City, UT 84112, USA
4 ARUP Institute for Clinical and Experimental Pathology, Salt Lake City, UT, USA
5 Department of Genetic Medicine, Weill Cornell Medical College in Qatar, Doha, Qatar
3 Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84112, USA
2 Cardiovascular Genetics Division, University of Utah School of Medicine, Salt Lake City, UT 84112, USA
AuthorAffiliation_xml – name: 1 Department of Human Genetics, University of Utah School of Medicine, Salt Lake City, UT 84112, USA
– name: 2 Cardiovascular Genetics Division, University of Utah School of Medicine, Salt Lake City, UT 84112, USA
– name: 4 ARUP Institute for Clinical and Experimental Pathology, Salt Lake City, UT, USA
– name: 3 Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84112, USA
– name: 5 Department of Genetic Medicine, Weill Cornell Medical College in Qatar, Doha, Qatar
Author_xml – sequence: 1
  fullname: Adams, Ted D.
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/26881067$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright Copyright © 2015 Sandra J. Hasstedt et al.
COPYRIGHT 2015 John Wiley & Sons, Inc.
COPYRIGHT 2016 John Wiley & Sons, Inc.
Copyright © 2015 Sandra J. Hasstedt et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright © 2015 Sandra J. Hasstedt et al. 2015
Copyright_xml – notice: Copyright © 2015 Sandra J. Hasstedt et al.
– notice: COPYRIGHT 2015 John Wiley & Sons, Inc.
– notice: COPYRIGHT 2016 John Wiley & Sons, Inc.
– notice: Copyright © 2015 Sandra J. Hasstedt et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
– notice: Copyright © 2015 Sandra J. Hasstedt et al. 2015
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Snippet Background/Objectives. To identify copy number variants (CNVs) which are associated with body mass index (BMI). Subjects/Methods. CNVs were identified using...
Background/Objectives. To identify copy number variants (CNVs) which are associated with body mass index (BMI). Subjects/Methods. CNVs were identified using...
To identify copy number variants (CNVs) which are associated with body mass index (BMI). CNVs were identified using array comparative genomic hybridization...
[ProQuest: [...] denotes non US-ASCII text; see PDF] Background/Objectives. To identify copy number variants (CNVs) which are associated with body mass index...
To identify copy number variants (CNVs) which are associated with body mass index (BMI).BACKGROUND/OBJECTIVESTo identify copy number variants (CNVs) which are...
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StartPage 246
SubjectTerms ADP-Ribosylation Factors - genetics
Adult
Aged
Aged, 80 and over
Alleles
Analysis
Body Mass Index
Chromosomes
Chromosomes, Human, Pair 20
Colleges & universities
Comparative Genomic Hybridization
Copy number variations
Deoxyribonucleic acid
DNA
DNA Copy Number Variations
Drug dosages
Families & family life
Female
Genes
Genetic aspects
Genetic Pleiotropy
Genetic Predisposition to Disease
Genetic variation
Genetics
Genome-Wide Association Study
Genomes
Genomics
Genotype
Humans
Male
Medicine
Middle Aged
Obesity
Obesity, Morbid - genetics
Pedigree
Physiological aspects
Reference Values
Risk factors
Sequence Deletion
Software
Thinness - genetics
Young Adult
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Title A Copy Number Variant on Chromosome 20q13.3 Implicated in Thinness and Severe Obesity
URI https://www.airitilibrary.com/Article/Detail/P20151217004-201512-201703060003-201703060003-246-252
https://search.emarefa.net/detail/BIM-1069619
https://dx.doi.org/10.1155/2015/623431
https://www.ncbi.nlm.nih.gov/pubmed/26881067
https://www.proquest.com/docview/1755486129
https://www.proquest.com/docview/1765917114
https://pubmed.ncbi.nlm.nih.gov/PMC4736014
https://doaj.org/article/4b51710150f04d7aa0945b237bf1fd31
Volume 2015
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