{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T21:15:37Z","timestamp":1775078137003,"version":"3.50.1"},"reference-count":30,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2017,6,27]],"date-time":"2017-06-27T00:00:00Z","timestamp":1498521600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"UAE University","award":["NP-15-23"],"award-info":[{"award-number":["NP-15-23"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Human Genetics"],"published-print":{"date-parts":[[2017,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background and purpose<\/jats:title><jats:p>Individuals with slow N\u2010acetylation phenotype often experience toxicity from drugs such as isoniazid, sulfonamides, procainamide, and hydralazine, whereas rapid acetylators may not respond to these medications. The highly polymorphic N\u2010acetyltransferase 2 enzyme encoded by the <jats:italic>NAT2<\/jats:italic> gene is one of the N\u2010acetylators in humans with a clear impact on the metabolism of a significant number of important drugs. However, there are limited studies on N\u2010acetylation phenotypes and <jats:italic>NAT2<\/jats:italic> genotypes among Emiratis, and thus this study was carried out to fill this gap.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Five hundred seventy\u2010six Emirati subjects were asked to consume a soft drink containing caffeine (a nontoxic and reliable probe for predicting the acetylation phenotype) and then provide a buccal swab along with a spot urine sample. Polymerase chain reaction\u2013restriction fragment length polymorphism (PCR\u2010RFLP) was used to determine the genotype of each individual. Phenotyping was carried out by analyzing the caffeine metabolites using high\u2010performance liquid chromatography (HPLC) analysis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We found that 78.5%, 19.1%, and 2.4% of the Emirati subjects were slow, intermediate, and rapid acetylators, respectively. In addition, we found that 77.4% of the subjects were homozygous or heterozygous for two nonreference alleles, whereas 18.4% and 4.2% were heterozygous or homozygous for the reference allele (<jats:italic>NAT2<\/jats:italic>*4), respectively. The most common genotypes found were <jats:italic>NAT2*5B\/*7B<\/jats:italic>, <jats:italic>NAT2<\/jats:italic>*<jats:italic>5B\/*6A<\/jats:italic>, <jats:italic>NAT2*7B\/*14B<\/jats:italic>, and <jats:italic>NAT2*4\/*5B<\/jats:italic>, with frequencies of 0.255, 0.135, 0.105, and 0.09, respectively. The degree of phenotype\/genotype concordance was 96.2%. The <jats:italic>NAT2*6A\/*6A<\/jats:italic>, <jats:italic>NAT2*6A\/*7B<\/jats:italic>, <jats:italic>NAT2*7B\/*7B<\/jats:italic>, and <jats:italic>NAT2*5A\/*5B<\/jats:italic> genotypes were found to be associated with the lowest 5\u2010acetylamino\u20106\u2010formylamino\u20103\u2010methyluracil\/1\u2010methylxanthine (AFMU\/1X) ratios.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>There is a high percentage of slow acetylators among Emiratis, which correlates with the presence of nonreference alleles for the <jats:italic>NAT2<\/jats:italic> gene. Individuals who carried <jats:italic>NAT2*6A\/*6A, NAT2*6A\/*7B, NAT2*7B\/*7B, or NAT2*5A\/*5B<\/jats:italic> genotypes might be at higher risk of toxicity with some drugs and some diseases compared to others, as these genotypes are associated with the slowest acetylation status.<\/jats:p><\/jats:sec>","DOI":"10.1111\/ahg.12198","type":"journal-article","created":{"date-parts":[[2017,6,27]],"date-time":"2017-06-27T10:48:40Z","timestamp":1498560520000},"page":"190-196","source":"Crossref","is-referenced-by-count":9,"title":["Studies on N\u2010Acetyltransferase (NAT2) Genotype Relationships in Emiratis: Confirmation of the Existence of Phenotype Variation among Slow Acetylators"],"prefix":"10.1111","volume":"81","author":[{"given":"Mohammad M.","family":"Al\u2010Ahmad","sequence":"first","affiliation":[{"name":"Department of Pharmacology, College of Medicine and Health Sciences UAE University  Al Ain United Arab 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United Arab Emirates"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bassam R.","family":"Ali","sequence":"additional","affiliation":[{"name":"Department of Pathology, College of Medicine and Health Sciences UAE University  Al Ain United Arab Emirates"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4771-7140","authenticated-orcid":false,"given":"Salim","family":"Bastaki","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, College of Medicine and Health Sciences UAE University  Al Ain United Arab Emirates"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2017,6,27]]},"reference":[{"key":"e_1_2_14_2_1","doi-asserted-by":"publisher","DOI":"10.1373\/clinchem.2008.105569"},{"key":"e_1_2_14_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1383-5718(00)00049-8"},{"key":"e_1_2_14_4_1","first-page":"165","volume-title":"Analyses of Hazardous 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