What you carry at this position in your DNA and what research says about it.
Insulin Sensitivity: 5/10 evidence, 20 publications.
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Sample genotype (not yours): G/G
Typical Insulin Sensitivity but Higher Drug Toxicity Risk
Typical insulin sensitivity is expected with this genetic profile, helping to maintain healthy blood sugar levels. However, this genotype is linked to a higher risk of toxicity from certain medications like isoniazid and phenytoin.
What this genotype means: Typical insulin sensitivity; Increased risk of isoniazid toxicity; Increased risk of phenytoin toxicity.
Sample genotype (not yours): A/A
Increased Insulin Resistance but Typical Drug Toxicity Risk
An increased risk of insulin resistance is associated with this genetic profile, making metabolic health a priority. Fortunately, you have a typical risk profile for toxicities from medications like isoniazid and phenytoin.
What this genotype means: Increased risk of insulin resistance; Typical risk of isoniazid toxicity; Typical risk of phenytoin toxicity.
Sample genotype (not yours): G/A
Increased Insulin Resistance and Higher Drug Toxicity Risk
An increased risk of insulin resistance is associated with this genetic profile, which may affect blood sugar regulation. Additionally, this genotype is linked to a higher likelihood of drug-induced toxicities.
What this genotype means: Increased risk of insulin resistance; Increased risk of isoniazid toxicity; Increased risk of phenytoin toxicity.
Gene function and biological role
Gene Function: The NAT2 gene encodes N-acetyltransferase 2, a crucial Phase II liver enzyme responsible for metabolizing various drugs, environmental toxins, and carcinogens [1]. This enzyme classifies individuals into rapid, intermediate, or slow acetylators based on how quickly they process these substances [2]. Beyond its classic role in drug clearance, NAT2 has been identified as a key player in metabolic health and systemic insulin sensitivity [3]. Genetic variations in this gene can alter enzyme stability, substrate binding, and overall metabolic efficiency [4].
Variant Impact: The rs1208 variant is a missense mutation in the NAT2 gene that changes the amino acid at position 268 from arginine to lysine [5]. This specific change alters the structural dynamics of the N-acetyltransferase 2 enzyme, influencing its metabolic rate [4]. While the ancestral allele is associated with rapid drug clearance, it unexpectedly increases the risk of metabolic dysfunction [3]. This variant is highly prevalent across global populations, with frequency patterns varying significantly by ancestry [6].
Key Insight: While the G allele speeds up drug detoxification, it surprisingly protects against insulin resistance. Conversely, the A allele improves drug safety profiles but increases metabolic risks.
Location: NAT2. Chromosome 8 · 8p22 · 18.4 Mb
Estimated prevalence by population
Global 16.4%; European 18.1%; African 16.0%; East Asian 0.2%; South Asian 12.3%; Americas 13.3%; Ashkenazi 19.4%; Finnish 20.0%; Middle Eastern 22.0%; Amish 10.4%.
Estimated GG genotype frequency.
Global 46.9%; European 48.9%; African 48.0%; East Asian 7.7%; South Asian 45.5%; Americas 46.4%; Ashkenazi 49.3%; Finnish 49.4%; Middle Eastern 49.8%; Amish 43.7%.
Estimated GA genotype frequency.
Global 36.8%; European 33.0%; African 36.0%; East Asian 92.2%; South Asian 42.1%; Americas 40.3%; Ashkenazi 31.3%; Finnish 30.6%; Middle Eastern 28.2%; Amish 45.8%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Metabolic Syndrome & Insulin Resistance
Insulin Resistance. Evidence: 3/10. Source: PMID 25798622. Typical Risk.
Pharmacogenomics
Antimicrobial & Antiviral Response
Isoniazid Toxicity. Evidence: 5/10. Source: PMID 27488001. Increased Risk.
Antiepileptic & Mood-Stabilizer Response
Phenytoin Toxicity. Evidence: 5/10. Source: PMID 27488001. Increased Risk.
Cancer & Oncology
Cancer Prognosis & Treatment Outcome
Paclitaxel Survival. Evidence: 5/10. Source: PMID 34911343. Decreased Survival.
Platinum Chemotherapy Survival. Evidence: 5/10. Source: PMID 34911343. Decreased Survival.
Showing effects for A/A genotype
Insulin Resistance. Evidence: 3/10. Source: PMID 25798622. Increased Risk.
Isoniazid Toxicity. Evidence: 5/10. Source: PMID 27488001. Typical Risk.
Phenytoin Toxicity. Evidence: 5/10. Source: PMID 27488001. Typical Risk.
Paclitaxel Survival. Evidence: 5/10. Source: PMID 34911343. Typical Survival.
Platinum Chemotherapy Survival. Evidence: 5/10. Source: PMID 34911343. Typical Survival.
Showing effects for G/A genotype
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Typical insulin sensitivity is characteristic of the G/G genotype, helping your body process glucose efficiently and lowering your baseline risk for insulin resistance [1]. However, in pharmacogenomics, the G allele is associated with rapid acetylation that can paradoxically increase the risk of adverse reactions or altered drug survival [2]. Specifically, studies show that individuals with this genotype have an increased risk of drug toxicity when taking isoniazid or phenytoin [3]. Furthermore, patients undergoing chemotherapy with paclitaxel or platinum compounds have shown decreased survival rates when carrying this genotype [4]. Understanding these genetic tendencies can help healthcare providers tailor medication choices and dosages to optimize safety and efficacy [5]. This knowledge allows for proactive discussions with your medical team regarding personalized treatment plans. Ultimately, being aware of these metabolic and drug-processing traits empowers you to make informed lifestyle and healthcare decisions.
Typical insulin sensitivity; Increased risk of isoniazid toxicity; Increased risk of phenytoin toxicity; Decreased survival with paclitaxel and platinum chemotherapy.
Sample genotype: AA (Homozygous)
Decreased insulin sensitivity is strongly linked to the A/A genotype, which can elevate your risk for insulin resistance and related metabolic conditions [1]. This effect on insulin sensitivity is independent of body mass index, suggesting a direct genetic influence on glucose metabolism [1]. On the positive side, the A/A genotype does not carry the elevated drug toxicity risks associated with the G allele [2]. Individuals with this genotype typically experience standard clearance rates and typical survival outcomes when treated with isoniazid, phenytoin, paclitaxel, or platinum compounds [3]. Your pharmacogenomic profile for these specific medications is generally favorable [4].
Increased risk of insulin resistance; Typical risk of isoniazid toxicity; Typical risk of phenytoin toxicity; Typical survival with paclitaxel and platinum chemotherapy.
Sample genotype: GA (Heterozygous)
An increased risk for insulin resistance is associated with the G/A genotype, as the A allele is linked to reduced insulin sensitivity independent of body mass index [1]. On the medication side, the G allele continues to expose you to rapid-acetylator drug risks [2]. Clinical studies have shown that individuals with the G/A genotype experience an increased risk of drug toxicity when treated with isoniazid or phenytoin [3]. Additionally, this genotype is associated with decreased survival times in patients receiving paclitaxel or platinum-based chemotherapies [4]. These findings highlight a complex genetic profile where metabolic risks and drug sensitivities coexist, making personalized healthcare strategies particularly valuable [5]. Discussing these results with your doctor can help guide safer prescribing practices. Ultimately, monitoring your metabolic health through regular check-ups remains a key step in managing these genetic risks.
Increased risk of insulin resistance; Increased risk of isoniazid toxicity; Increased risk of phenytoin toxicity; Decreased survival with paclitaxel and platinum chemotherapy.
Variants with shared genetic architecture
rs1495741 · NAT2 Gene · Chr 8 · Drug and Toxin Metabolism
rs1041983 · NAT2 Gene · Chr 8 · Drug Metabolism Speed
rs1495743 · NAT2 Gene · Chr 8 · Cholesterol Levels
Identification and validation of N-acetyltransferase 2 as an insulin sensitivity gene.
Structure/function evaluations of single nucleotide polymorphisms in human N-acetyltransferase 2.
Multiple advantageous amino acid variants in the NAT2 gene in human populations.
Genotyping panel for assessing response to cancer chemotherapy.
Content updated August 2026.
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