What you carry at this position in your DNA and what research says about it.
Type 2 Diabetes Risk: 9/10 evidence, 43 publications.
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Sample genotype (not yours): C/C
Higher Risk of Type 2 Diabetes
Carrying two copies of the C allele is linked to a higher risk of developing type 2 diabetes due to reduced insulin secretion. Standard diabetes medications like repaglinide and gliclazide show typical, baseline effectiveness.
What this genotype means: Elevated risk of developing type 2 diabetes; Lower insulin secretion in response to glucose; Typical response to repaglinide and gliclazide therapies.
Sample genotype (not yours): C/T
Slightly Higher Risk of Type 2 Diabetes
Carrying one copy of the C allele is associated with a moderate increase in type 2 diabetes risk. However, this genotype is also linked to an improved response to certain blood sugar-lowering medications.
What this genotype means: Moderately elevated risk of type 2 diabetes; Slightly reduced early-phase insulin secretion; Enhanced blood sugar-lowering response to repaglinide and gliclazide.
Sample genotype (not yours): T/T
Lower Risk of Type 2 Diabetes
Carrying two copies of the T allele provides significant protection against type 2 diabetes. Additionally, this genotype is associated with a highly favorable response to specific diabetes medications.
What this genotype means: Significantly lower risk of developing type 2 diabetes; More efficient insulin secretion and glucose clearance; Excellent therapeutic response to repaglinide and gliclazide.
Gene function and biological role
Gene Function: The KCNQ1 gene encodes a crucial component of voltage-gated potassium channels that regulate electrical activity in various tissues [1]. While highly famous for its role in controlling the electrical rhythm of the heart, this channel is also active in the insulin-producing beta cells of the pancreas [2]. In these pancreatic cells, the channel helps manage the electrical signals that trigger insulin release in response to glucose [3]. Variations in how this gene is expressed can alter the timing and amount of insulin secreted after eating, directly impacting blood sugar control [3].
Variant Impact: Located within an intron of the KCNQ1 gene, rs2237892 is a common genetic variant that influences susceptibility to metabolic conditions [1]. The change from a T allele to a C allele is strongly associated with impaired pancreatic beta-cell function and reduced insulin secretion [3]. This molecular shift alters the body's early-phase insulin response, making it harder to clear glucose from the bloodstream after meals [2]. Consequently, this variant has emerged as one of the most significant genetic risk factors for metabolic dysfunction, particularly in East Asian populations [1].
Key Insight: The same genetic channel that regulates your heartbeat also controls how your pancreas releases insulin in response to a meal.
Location: KCNQ1. Chromosome 11 · 11p15.4 · 2.8 Mb
Estimated prevalence by population
Global 82.1%; European 88.1%; African 80.9%; East Asian 43.0%; South Asian 94.2%; Americas 61.0%; Ashkenazi 89.0%; Finnish 89.2%; Middle Eastern 89.4%; Amish 94.8%.
Estimated CC genotype frequency.
Global 16.5%; European 11.5%; African 18.1%; East Asian 45.1%; South Asian 5.7%; Americas 34.2%; Ashkenazi 10.7%; Finnish 10.5%; Middle Eastern 10.3%; Amish 5.1%.
Estimated CT genotype frequency.
Global 1.4%; European 0.4%; African 1.0%; East Asian 11.8%; South Asian 0.1%; Americas 4.8%; Ashkenazi 0.3%; Finnish 0.3%; Middle Eastern 0.3%; Amish 0.1%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Cardiovascular & Metabolic
Diabetes & Glycemic Traits
Type 2 Diabetes. Evidence: 9/10. Source: PMID 18711367. ~1.3x Higher Risk.
Obesity & Body Composition
Body Mass Index. Evidence: 6/10. Source: PMID 24861553. Typical BMI.
Pharmacogenomics
Diabetes Medication Response
Repaglinide Response. Evidence: 5/10. Source: PMID 22414228. Typical Response.
Gliclazide Response. Evidence: 5/10. Source: PMID 27694910. Typical Response.
Showing effects for C/T genotype
Type 2 Diabetes. Evidence: 9/10. Source: PMID 18711367. Slightly Higher Risk.
Repaglinide Response. Evidence: 5/10. Source: PMID 22414228. Stronger Response.
Gliclazide Response. Evidence: 5/10. Source: PMID 27694910. Stronger Response.
Showing effects for T/T genotype
Type 2 Diabetes. Evidence: 9/10. Source: PMID 18711367. Lower Risk.
Body Mass Index. Evidence: 6/10. Source: PMID 24861553. Slightly Higher BMI.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Inheriting two copies of the C allele places an individual at the highest genetic risk tier for type 2 diabetes at this locus [1]. Large-scale genome-wide association studies show a consistent link between this genotype and impaired pancreatic beta-cell function [2]. The pancreas struggles to release sufficient insulin quickly after glucose intake, leading to higher post-meal blood sugar levels [3]. While this is the most common genotype globally, it represents a metabolic vulnerability that requires proactive lifestyle management. On the therapeutic side, clinical studies indicate a standard or typical response to common oral diabetes medications such as repaglinide [4]. Maintaining a balanced diet and regular physical activity are particularly beneficial for mitigating this genetic predisposition.
Elevated risk of developing type 2 diabetes; Lower insulin secretion in response to glucose; Typical response to repaglinide and gliclazide therapies.
Sample genotype: CT (Heterozygous)
Possessing one copy of the risk-associated C allele and one copy of the protective T allele results in an intermediate metabolic profile [1]. There is still a slightly elevated risk of developing type 2 diabetes compared to those with two protective alleles [2]. This is driven by a mild reduction in early-phase insulin secretion when blood sugar rises [3]. Interestingly, clinical trials have shown that carriers of this genotype respond better to certain oral antidiabetic medications [4]. Specifically, drugs like repaglinide and gliclazide show enhanced efficacy in lowering blood sugar and improving insulin sensitivity [4]. This means that if medical treatment is ever required, standard therapies may be highly effective.
Moderately elevated risk of type 2 diabetes; Slightly reduced early-phase insulin secretion; Enhanced blood sugar-lowering response to repaglinide and gliclazide.
Sample genotype: TT (Homozygous)
Inheriting two copies of the T allele is highly protective against the development of type 2 diabetes [1]. This genotype is associated with robust pancreatic beta-cell function and efficient insulin release after meals [2]. Because the pancreas secretes insulin effectively, blood sugar levels are cleared from the bloodstream more efficiently [3]. Although this protective genotype is relatively rare in European populations, it is more common in East Asian ancestries [1]. In the event that diabetes does develop, clinical research indicates that these individuals have an exceptionally strong response to medications like repaglinide and gliclazide [4]. These drugs work in harmony with the potassium channel to optimize insulin sensitivity and glucose control [4].
Significantly lower risk of developing type 2 diabetes; More efficient insulin secretion and glucose clearance; Excellent therapeutic response to repaglinide and gliclazide.
Variants with shared genetic architecture
rs2074238 · KCNQ1 Gene · Chr 11 · Cardiac QT Interval
rs2237895 · KCNQ1 Gene · Chr 11 · Type 2 Diabetes Risk
rs2237897 · KCNQ1 Gene · Chr 11 · Type 2 Diabetes Risk
Variants in KCNQ1 are associated with susceptibility to type 2 diabetes mellitus.
Association of type 2 diabetes candidate polymorphisms in KCNQ1 with incretin and insulin secretion.
Content updated August 2026.
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