FAM13A affects body fat distribution and adipocyte function
Genetic variation in the FAM13A (Family with Sequence Similarity 13 Member A) locus has been associated with several glycemic and metabolic traits in genome-wide association studies (GWAS). Here, we demonstrate that in humans, FAM13A alleles are associated with increased FAM13A expression in subcuta...
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| Published in: | Nature communications Vol. 11; no. 1; pp. 1465 - 13 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
London
Nature Publishing Group UK
19.03.2020
Nature Publishing Group Nature Portfolio |
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| ISSN: | 2041-1723, 2041-1723 |
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| Abstract | Genetic variation in the
FAM13A
(Family with Sequence Similarity 13 Member A) locus has been associated with several glycemic and metabolic traits in genome-wide association studies (GWAS). Here, we demonstrate that in humans,
FAM13A
alleles are associated with increased
FAM13A
expression in subcutaneous adipose tissue (SAT) and an insulin resistance-related phenotype (e.g. higher waist-to-hip ratio and fasting insulin levels, but lower body fat). In human adipocyte models, knockdown of
FAM13A
in preadipocytes accelerates adipocyte differentiation. In mice,
Fam13a
knockout (KO) have a lower visceral to subcutaneous fat (VAT/SAT) ratio after high-fat diet challenge, in comparison to their wild-type counterparts. Subcutaneous adipocytes in KO mice show a size distribution shift toward an increased number of smaller adipocytes, along with an improved adipogenic potential. Our results indicate that GWAS-associated variants within the
FAM13A
locus alter adipose
FAM13A
expression, which in turn, regulates adipocyte differentiation and contribute to changes in body fat distribution.
Genetic variants in the
FAM13A
locus have been associated with anthropometric and glycemic traits. Here, using fine-mapping, in vitro knockdown studies in pre-adipocytes and in vivo knockout in mice, the authors show that FAM13A is involved in regulating fat distribution and metabolic traits. |
|---|---|
| AbstractList | Genetic variation in the
FAM13A
(Family with Sequence Similarity 13 Member A) locus has been associated with several glycemic and metabolic traits in genome-wide association studies (GWAS). Here, we demonstrate that in humans,
FAM13A
alleles are associated with increased
FAM13A
expression in subcutaneous adipose tissue (SAT) and an insulin resistance-related phenotype (e.g. higher waist-to-hip ratio and fasting insulin levels, but lower body fat). In human adipocyte models, knockdown of
FAM13A
in preadipocytes accelerates adipocyte differentiation. In mice,
Fam13a
knockout (KO) have a lower visceral to subcutaneous fat (VAT/SAT) ratio after high-fat diet challenge, in comparison to their wild-type counterparts. Subcutaneous adipocytes in KO mice show a size distribution shift toward an increased number of smaller adipocytes, along with an improved adipogenic potential. Our results indicate that GWAS-associated variants within the
FAM13A
locus alter adipose
FAM13A
expression, which in turn, regulates adipocyte differentiation and contribute to changes in body fat distribution.
Genetic variants in the
FAM13A
locus have been associated with anthropometric and glycemic traits. Here, using fine-mapping, in vitro knockdown studies in pre-adipocytes and in vivo knockout in mice, the authors show that FAM13A is involved in regulating fat distribution and metabolic traits. Genetic variation in the FAM13A (Family with Sequence Similarity 13 Member A) locus has been associated with several glycemic and metabolic traits in genome-wide association studies (GWAS). Here, we demonstrate that in humans, FAM13A alleles are associated with increased FAM13A expression in subcutaneous adipose tissue (SAT) and an insulin resistance-related phenotype (e.g. higher waist-to-hip ratio and fasting insulin levels, but lower body fat). In human adipocyte models, knockdown of FAM13A in preadipocytes accelerates adipocyte differentiation. In mice, Fam13a knockout (KO) have a lower visceral to subcutaneous fat (VAT/SAT) ratio after high-fat diet challenge, in comparison to their wild-type counterparts. Subcutaneous adipocytes in KO mice show a size distribution shift toward an increased number of smaller adipocytes, along with an improved adipogenic potential. Our results indicate that GWAS-associated variants within the FAM13A locus alter adipose FAM13A expression, which in turn, regulates adipocyte differentiation and contribute to changes in body fat distribution. Genetic variation in the FAM13A (Family with Sequence Similarity 13 Member A) locus has been associated with several glycemic and metabolic traits in genome-wide association studies (GWAS). Here, we demonstrate that in humans, FAM13A alleles are associated with increased FAM13A expression in subcutaneous adipose tissue (SAT) and an insulin resistance-related phenotype (e.g. higher waist-to-hip ratio and fasting insulin levels, but lower body fat). In human adipocyte models, knockdown of FAM13A in preadipocytes accelerates adipocyte differentiation. In mice, Fam13a knockout (KO) have a lower visceral to subcutaneous fat (VAT/SAT) ratio after high-fat diet challenge, in comparison to their wild-type counterparts. Subcutaneous adipocytes in KO mice show a size distribution shift toward an increased number of smaller adipocytes, along with an improved adipogenic potential. Our results indicate that GWAS-associated variants within the FAM13A locus alter adipose FAM13A expression, which in turn, regulates adipocyte differentiation and contribute to changes in body fat distribution.Genetic variation in the FAM13A (Family with Sequence Similarity 13 Member A) locus has been associated with several glycemic and metabolic traits in genome-wide association studies (GWAS). Here, we demonstrate that in humans, FAM13A alleles are associated with increased FAM13A expression in subcutaneous adipose tissue (SAT) and an insulin resistance-related phenotype (e.g. higher waist-to-hip ratio and fasting insulin levels, but lower body fat). In human adipocyte models, knockdown of FAM13A in preadipocytes accelerates adipocyte differentiation. In mice, Fam13a knockout (KO) have a lower visceral to subcutaneous fat (VAT/SAT) ratio after high-fat diet challenge, in comparison to their wild-type counterparts. Subcutaneous adipocytes in KO mice show a size distribution shift toward an increased number of smaller adipocytes, along with an improved adipogenic potential. Our results indicate that GWAS-associated variants within the FAM13A locus alter adipose FAM13A expression, which in turn, regulates adipocyte differentiation and contribute to changes in body fat distribution. Genetic variation in the FAM13A (Family with Sequence Similarity 13 Member A) locus has been associated with several glycemic and metabolic traits in genome-wide association studies (GWAS). Here, we demonstrate that in humans, FAM13A alleles are associated with increased FAM13A expression in subcutaneous adipose tissue (SAT) and an insulin resistance-related phenotype (e.g. higher waist-to-hip ratio and fasting insulin levels, but lower body fat). In human adipocyte models, knockdown of FAM13A in preadipocytes accelerates adipocyte differentiation. In mice, Fam13a knockout (KO) have a lower visceral to subcutaneous fat (VAT/SAT) ratio after high-fat diet challenge, in comparison to their wild-type counterparts. Subcutaneous adipocytes in KO mice show a size distribution shift toward an increased number of smaller adipocytes, along with an improved adipogenic potential. Our results indicate that GWAS-associated variants within the FAM13A locus alter adipose FAM13A expression, which in turn, regulates adipocyte differentiation and contribute to changes in body fat distribution. Genetic variants in the FAM13A locus have been associated with anthropometric and glycemic traits. Here, using fine-mapping, in vitro knockdown studies in pre-adipocytes and in vivo knockout in mice, the authors show that FAM13A is involved in regulating fat distribution and metabolic traits. Genetic variation in the FAM13A (Family with Sequence Similarity 13 Member A) locus has been associated with several glycemic and metabolic traits in genome-wide association studies (GWAS). Here, we demonstrate that in humans, FAM13A alleles are associated with increased FAM13A expression in subcutaneous adipose tissue (SAT) and an insulin resistance-related phenotype (e.g. higher waist-to-hip ratio and fasting insulin levels, but lower body fat). In human adipocyte models, knockdown of FAM13A in preadipocytes accelerates adipocyte differentiation. In mice, Fam13a knockout (KO) have a lower visceral to subcutaneous fat (VAT/SAT) ratio after high-fat diet challenge, in comparison to their wild-type counterparts. Subcutaneous adipocytes in KO mice show a size distribution shift toward an increased number of smaller adipocytes, along with an improved adipogenic potential. Our results indicate that GWAS-associated variants within the FAM13A locus alter adipose FAM13A expression, which in turn, regulates adipocyte differentiation and contribute to changes in body fat distribution.Genetic variants in the FAM13A locus have been associated with anthropometric and glycemic traits. Here, using fine-mapping, in vitro knockdown studies in pre-adipocytes and in vivo knockout in mice, the authors show that FAM13A is involved in regulating fat distribution and metabolic traits. Genetic variation in the FAM13A (Family with Sequence Similarity 13 Member A) locus has been associated with several glycemic and metabolic traits in genome-wide association studies (GWAS). Here, we demonstrate that in humans, FAM13A alleles are associated with increased FAM13A expression in subcutaneous adipose tissue (SAT) and an insulin resistance-related phenotype (e.g. higher waist-to-hip ratio and fasting insulin levels, but lower body fat). In human adipocyte models, knockdown of FAM13A in preadipocytes accelerates adipocyte differentiation. In mice, Fam13a knockout (KO) have a lower visceral to subcutaneous fat (VAT/SAT) ratio after high-fat diet challenge, in comparison to their wild-type counterparts. Subcutaneous adipocytes in KO mice show a size distribution shift toward an increased number of smaller adipocytes, along with an improved adipogenic potential. Our results indicate that GWAS-associated variants within the FAM13A locus alter adipose FAM13A expression, which in turn, regulates adipocyte differentiation and contribute to changes in body fat distribution. Genetic variants in the FAM13A locus have been associated with anthropometric and glycemic traits. Here, using fine-mapping, in vitro knockdown studies in pre-adipocytes and in vivo knockout in mice, the authors show that FAM13A is involved in regulating fat distribution and metabolic traits. |
| ArticleNumber | 1465 |
| Author | Rao, Abhiram Quertermous, Thomas Chennamsetty, Indumathi Zhou, Xiang Reilly, Dermot Wabitsch, Martin Seldin, Marcus Li, Jiehan Cook, Naomi Knowles, Joshua W. Attie, Allan Tada, Yuko McLaughlin, Tracey Ingelsson, Erik Gloudemans, Michael J. Keller, Mark Shin, Myung Kyun Fathzadeh, Mohsen Reaven, Gerald Carcamo-Orive, Ivan Molony, Cliona M. Montgomery, Stephen B. Lusis, Aldons J. Sangwung, Panjamaporn Yang, Jing |
| Author_xml | – sequence: 1 givenname: Mohsen orcidid: 0000-0002-7962-9148 surname: Fathzadeh fullname: Fathzadeh, Mohsen organization: Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford Cardiovascular Institute, Stanford University, Stanford Diabetes Research Center, Stanford University – sequence: 2 givenname: Jiehan surname: Li fullname: Li, Jiehan organization: Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford Cardiovascular Institute, Stanford University, Stanford Diabetes Research Center, Stanford University – sequence: 3 givenname: Abhiram surname: Rao fullname: Rao, Abhiram organization: Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Bioengineering Department, School of Engineering and Medicine – sequence: 4 givenname: Naomi orcidid: 0000-0002-1830-2432 surname: Cook fullname: Cook, Naomi organization: Department of Medical Sciences, Molecular Epidemiology, Uppsala University – sequence: 5 givenname: Indumathi surname: Chennamsetty fullname: Chennamsetty, Indumathi organization: Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford Cardiovascular Institute, Stanford University – sequence: 6 givenname: Marcus orcidid: 0000-0001-8026-4759 surname: Seldin fullname: Seldin, Marcus organization: Department of Human Genetics, David Geffen School of Medicine, UCLA – sequence: 7 givenname: Xiang surname: Zhou fullname: Zhou, Xiang organization: Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford Cardiovascular Institute, Stanford University – sequence: 8 givenname: Panjamaporn orcidid: 0000-0002-8145-7947 surname: Sangwung fullname: Sangwung, Panjamaporn organization: Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford Cardiovascular Institute, Stanford University, Stanford Diabetes Research Center, Stanford University – sequence: 9 givenname: Michael J. orcidid: 0000-0002-9924-9943 surname: Gloudemans fullname: Gloudemans, Michael J. organization: Department of Genetics, Stanford University – sequence: 10 givenname: Mark surname: Keller fullname: Keller, Mark organization: Department of Biochemistry, University of Wisconsin – sequence: 11 givenname: Allan orcidid: 0000-0002-0568-2261 surname: Attie fullname: Attie, Allan organization: Department of Biochemistry, University of Wisconsin – sequence: 12 givenname: Jing orcidid: 0000-0002-4983-1660 surname: Yang fullname: Yang, Jing organization: Department of Comparative Biosciences, College of Veterinary Medicine, University of Illinois at Urbana–Champaign – sequence: 13 givenname: Martin surname: Wabitsch fullname: Wabitsch, Martin organization: Division of Paediatric Endocrinology and Diabetes, Department of Paediatrics and Adolescent Medicine, University of Ulm – sequence: 14 givenname: Ivan orcidid: 0000-0001-8823-4925 surname: Carcamo-Orive fullname: Carcamo-Orive, Ivan organization: Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford Cardiovascular Institute, Stanford University, Stanford Diabetes Research Center, Stanford University – sequence: 15 givenname: Yuko orcidid: 0000-0003-1410-9894 surname: Tada fullname: Tada, Yuko organization: Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford Cardiovascular Institute, Stanford University – sequence: 16 givenname: Aldons J. orcidid: 0000-0001-9013-0228 surname: Lusis fullname: Lusis, Aldons J. organization: Department of Human Genetics, David Geffen School of Medicine, UCLA – sequence: 17 givenname: Myung Kyun surname: Shin fullname: Shin, Myung Kyun organization: Genetics and Pharmacogenomics, Merck & Co., Inc – sequence: 18 givenname: Cliona M. surname: Molony fullname: Molony, Cliona M. organization: Genetics and Pharmacogenomics, Merck & Co., Inc – sequence: 19 givenname: Tracey surname: McLaughlin fullname: McLaughlin, Tracey organization: Stanford Diabetes Research Center, Stanford University, Department of Medicine, Division of Endocrinology, Stanford University School of Medicine – sequence: 20 givenname: Gerald surname: Reaven fullname: Reaven, Gerald organization: Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford Cardiovascular Institute, Stanford University, Stanford Diabetes Research Center, Stanford University – sequence: 21 givenname: Stephen B. orcidid: 0000-0002-5200-3903 surname: Montgomery fullname: Montgomery, Stephen B. organization: Stanford Diabetes Research Center, Stanford University, Department of Genetics, Stanford University, Department of Medicine, Division of Endocrinology, Stanford University School of Medicine, Department of Pathology, Stanford University – sequence: 22 givenname: Dermot orcidid: 0000-0002-9456-1364 surname: Reilly fullname: Reilly, Dermot organization: Genetics and Pharmacogenomics, Merck & Co., Inc – sequence: 23 givenname: Thomas orcidid: 0000-0002-7645-9067 surname: Quertermous fullname: Quertermous, Thomas organization: Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford Cardiovascular Institute, Stanford University, Stanford Diabetes Research Center, Stanford University – sequence: 24 givenname: Erik orcidid: 0000-0003-2256-6972 surname: Ingelsson fullname: Ingelsson, Erik email: eriking@stanford.edu organization: Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford Cardiovascular Institute, Stanford University, Stanford Diabetes Research Center, Stanford University – sequence: 25 givenname: Joshua W. orcidid: 0000-0003-1922-7240 surname: Knowles fullname: Knowles, Joshua W. email: knowlej@stanford.edu organization: Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford Cardiovascular Institute, Stanford University, Stanford Diabetes Research Center, Stanford University |
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| Copyright_xml | – notice: The Author(s) 2020 – notice: The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| DOI | 10.1038/s41467-020-15291-z |
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| Snippet | Genetic variation in the
FAM13A
(Family with Sequence Similarity 13 Member A) locus has been associated with several glycemic and metabolic traits in... Genetic variation in the FAM13A (Family with Sequence Similarity 13 Member A) locus has been associated with several glycemic and metabolic traits in... Genetic variants in the FAM13A locus have been associated with anthropometric and glycemic traits. Here, using fine-mapping, in vitro knockdown studies in... |
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| SubjectTerms | 13/106 13/51 13/89 49/105 49/39 631/208/191/2018 631/208/205 631/443/319/1642 64/60 692/163/2743/393 82/1 96/1 Adipocytes Adipocytes - metabolism Adipogenesis - genetics Adipose tissue Animals Anthropometry Body fat Body Fat Distribution Cell Differentiation - genetics Differentiation Gene Knockdown Techniques Gene mapping Genetic diversity Genetic Loci Genetic variance Genome-wide association studies Genome-Wide Association Study GTPase-Activating Proteins - genetics GTPase-Activating Proteins - metabolism HEK293 Cells High fat diet Hip Humanities and Social Sciences Humans In vivo methods and tests Insulin Insulin resistance Insulin Resistance - genetics Intra-Abdominal Fat - metabolism Loci Male Mapping Metabolism Metabolomics Mice, Inbred C57BL Mice, Knockout multidisciplinary Phenotype Phenotypes Polymorphism, Single Nucleotide - genetics Preadipocytes RNA, Messenger - genetics RNA, Messenger - metabolism Science Science (multidisciplinary) Size distribution Subcutaneous Fat - metabolism |
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| Title | FAM13A affects body fat distribution and adipocyte function |
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