Identification and validation of N-acetyltransferase 2 as an insulin sensitivity gene
Open accessAbstract
Decreased insulin sensitivity, also referred to as insulin resistance (IR), is a fundamental abnormality in patients with type 2 diabetes and a risk factor for cardiovascular disease. While IR predisposition is heritable, the genetic basis remains largely unknown. The GENEticS of Insulin Sensitivity consortium conducted a genome-wide association study (GWAS) for direct measures of insulin sensitivity, such as euglycemic clamp or insulin suppression test, in 2,764 European individuals, with replication in an additional 2,860 individuals. The presence of a nonsynonymous variant of N-acetyltransferase 2 (NAT2) [rs1208 (803A>G, K268R)] was strongly associated with decreased insulin sensitivity that was independent of BMI. The rs1208 "A" allele was nominally associated with IR-related traits, including increased fasting glucose, hemoglobin A1C, total and LDL cholesterol, triglycerides, and coronary artery disease. NAT2 acetylates arylamine and hydrazine drugs and carcinogens, but predicted acetylator NAT2 phenotypes were not associated with insulin sensitivity. In a murine adipocyte cell line, silencing of NAT2 ortholog Nat1 decreased insulin-mediated glucose uptake, increased basal and isoproterenol-stimulated lipolysis, and decreased adipocyte differentiation, while Nat1 overexpression produced opposite effects. Nat1-deficient mice had elevations in fasting blood glucose, insulin, and triglycerides and decreased insulin sensitivity, as measured by glucose and insulin tolerance tests, with intermediate effects in Nat1 heterozygote mice. Our results support a role for NAT2 in insulin sensitivity.
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A study identified a single nucleotide polymorphism in N-acetyltransferase-2.
“A study by Knowles et al. (2015) identified a single nucleotide polymorphism in N-acetyltransferase-2 (mouse homolog is NAT-1).”
From Myosteatosis in the Context of Skeletal Muscle Function Deficit: An Interdisciplinary Workshop at the National Institute on Aging (2020) · cites this paper as Knowles et al., 2015
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- Authors
- Knowles, J. W., Xie, W., Zhang, Z., Chennemsetty, I., Assimes, T. L., Paananen, J., Hansson, O., Pankow, J., Goodarzi, M. O., Carcamo-Orive, I., Morris, A. P., Chen, Y.-D. I., Mäkinen, V.-P., Ganna, A., Mahajan, A., Guo, X., Abbasi, F., Greenawalt, D. M., Lum, P., Molony, C., Lind, L., Lindgren, C., Raffel, L. J., Tsao, P. S., Schadt, E. E., Rotter, J. I., Sinaiko, A., Reaven, G., Yang, X., Hsiung, C. A., Groop, L., Cordell, H. J., Laakso, M., Hao, K., Ingelsson, E., Frayling, T. M., Weedon, M. N., Walker, M., & Quertermous, T.
- Affiliations
- Stanford Cardiovascular Institute (US)
- University of Exeter (GB)
- Icahn School of Medicine at Mount Sinai (US)
- University of Eastern Finland (FI)
- Lund University (SE)
- University of Minnesota (US)
- Cedars-Sinai Medical Center (US)
- Centre for Human Genetics (GB)
- University of California, Los Angeles (US)
- Uppsala University (SE)
- Merck & Co., Inc., Rahway, NJ, USA (United States) (US)
- National Health Research Institutes (TW)
- Institute for Genetic Medicine, Hokkaido University (JP)
- Newcastle University (GB)
- Corresponding author
- Knowles, Joshua W.
- Xie, Weijia
- Zhang, Zhongyang
- Hao, Ke
- Ingelsson, Erik
- Frayling, Timothy M.
- Weedon, Michael N.
- Quertermous, Thomas
- ORCID
- Knowles, Joshua W.
- Xie, Weijia
- Zhang, Zhongyang
- Assimes, Themistocles L.
- Paananen, Jussi
- Hansson, Ola
- Pankow, James
- Goodarzi, Mark O.
- Morris, Andrew P.
- Chen, Yii-Der I.
- Mäkinen, Ville-Petteri
- Ganna, Andrea
- Mahajan, Anubha
- Guo, Xiuqing
- Abbasi, Fahim
- Lum, Pek
- Molony, Cliona
- Lind, Lars
- Lindgren, Cecilia
- Tsao, Philip S.
- Schadt, Eric E.
- Rotter, Jerome I.
- Sinaiko, Alan
- Yang, Xia
- Hsiung, Chao A.
- Cordell, Heather J.
- Laakso, Markku
- Hao, Ke
- Ingelsson, Erik
- Frayling, Timothy M.
- Weedon, Michael N.
- Walker, Mark
- Quertermous, Thomas
- Venue
- Journal of Clinical Investigation
- Published
- 2015-03-23
- Volume
- 125
- Issue
- 4
- Pages
- 1739-1751
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC4409020
- OpenAlex
- W2115675380
- Cited by
- 141
- References
- 66
- Citations by year
- 2026: 7 · 2025: 5 · 2024: 25 · 2023: 10 · 2022: 21 · 2021: 10 · 2020: 17 · 2019: 11 · 2018: 10 · 2017: 12 · 2016: 10 · 2015: 1 · 2014: 1
- FWCI
- 1.42
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Clinical Investigation (publishedVersion, public-domain)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- UEF eRepo (University of Eastern Finland) (submittedVersion, public-domain)
- eScholarship (California Digital Library) (submittedVersion)
- Figshare (submittedVersion)
- Lund University Publications (Lund University) (submittedVersion, other-oa)
- Open Research Exeter (University of Exeter) (submittedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Funders
- American Heart Association (10FTF3360005)
- AstraZeneca (QLG1-CT-2001-01252)
- Wellcome Trust (WT098017, 512013, 323195)
- European Commission (LSHM-CT-2004-512013, QLG1-CT-2001-01252)
- Fondation Leducq
- Stiftelsen för Strategisk Forskning
- Hjärt-Lungfonden
- Vetenskapsrådet
- National Health Research Institutes (PH-100-PP-03)
- National Institutes of Health (UL1TR000124)
- School of Medicine, Stanford University
- Stanford Bio-X
- National Heart, Lung, and Blood Institute (HL34659, R01HL034659, R01HL109512, R01HL052851, R33HL120757, HL-52851)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK072124, R01DK107437, DK085175, R01DK085175, R01DK072124, P60DK020541, P30DK063491, P30DK020541)
- National Center for Research Resources (M01RR000400, M01-RR00400)
- National Center for Advancing Translational Sciences
- Stanford Cardiovascular Institute, School of Medicine, Stanford University
- FP7 Ideas: European Research Council (323195)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Pharmacogenetics and Drug Metabolism
- Keywords
- N-acetyltransferase 2, NAT2, insulin sensitivity, insulin resistance, type 2 diabetes, genetic susceptibility, NAT1, adipocytes, glucose uptake, lipolysis, adipogenesis, fasting blood glucose, triglycerides, coronary artery disease, euglycemic clamp, insulin suppression test
- MeSH terms
- Adolescent, Adult, Animals, Arylamine N-Acetyltransferase, Child, Coronary Disease, Europe, Female, Gene Frequency, Glucose, Glycated Hemoglobin, Hispanic or Latino, Humans, Hyperglycemia, Insulin Resistance, Isoenzymes, Lipolysis, Male, Middle Aged, Prospective Studies, Taiwan, United States, Hypertriglyceridemia, Point Mutation, Mice, Knockout, Mutation, Missense, Polymorphism, Single Nucleotide, 3T3-L1 Cells, White People, Asian People, Adipogenesis, Mice, Genome-Wide Association Study, Young Adult
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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