What you carry at this position in your DNA and what research says about it.
Blood Sugar and Diabetes Risk: 10/10 evidence, 30 publications.
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Sample genotype (not yours): C/C
Typical Blood Sugar and Lower Diabetes Risk
Fasting glucose levels and HbA1c are within the typical baseline range. There is a lower risk of developing type 2 diabetes compared to carriers of the T allele.
What this genotype means: Typical fasting blood glucose levels; Lower risk of type 2 diabetes; Typical infant birth weight.
Sample genotype (not yours): C/T
Slightly Higher Blood Sugar and Diabetes Risk
Fasting blood glucose and HbA1c levels are slightly elevated. There is a moderately increased risk of developing type 2 diabetes.
What this genotype means: Slightly elevated fasting glucose; 1.3x increased risk of type 2 diabetes; Slightly higher infant birth weight.
Sample genotype (not yours): T/T
Elevated Blood Sugar and Higher Diabetes Risk
Fasting blood glucose and HbA1c levels are significantly higher. The risk of developing type 2 diabetes is elevated by nearly three-fold.
What this genotype means: Elevated fasting glucose levels; 2.7x increased risk of type 2 diabetes; Higher infant birth weight.
Gene function and biological role
Gene Function: Glucokinase, encoded by the GCK gene, serves as the primary glucose sensor in pancreatic beta-cells and hepatocytes [1]. It plays a critical role in maintaining glucose homeostasis by catalyzing the first step of glycolysis, phosphorylation of glucose to glucose-6-phosphate [1]. Variations in this gene can alter the threshold for insulin secretion, directly impacting fasting blood sugar levels [2]. While rare mutations in GCK cause monogenic forms of diabetes like MODY2, common regulatory variants subtly shift the metabolic setpoint [3].
Variant Impact: The rs1799884 variant is located in the beta-cell-specific promoter region of the GCK gene, specifically at the -30 position [4]. This single nucleotide change alters the transcriptional regulation of glucokinase, modifying how much of the enzyme is produced in response to glucose [2]. The minor T allele reduces promoter activity, leading to a higher threshold for insulin release and consequently elevated fasting blood glucose levels [3]. This regulatory shift also influences maternal glucose levels during pregnancy, which directly affects fetal growth and birth weight [5].
Key Insight: This variant acts as a genetic thermostat for blood sugar, adjusting the exact threshold at which the pancreas decides to release insulin.
Location: GCK. Chromosome 7 · 7p13 · 44.2 Mb
Estimated prevalence by population
Global 68.9%; European 68.7%; African 68.3%; East Asian 67.7%; South Asian 74.8%; Americas 64.7%; Ashkenazi 68.6%; Finnish 79.5%; Middle Eastern 56.8%; Amish 53.5%.
Estimated CC genotype frequency.
Global 28.1%; European 28.4%; African 28.7%; East Asian 29.2%; South Asian 23.4%; Americas 31.5%; Ashkenazi 28.4%; Finnish 19.3%; Middle Eastern 37.2%; Amish 39.3%.
Estimated CT genotype frequency.
Global 2.9%; European 2.9%; African 3.0%; East Asian 3.1%; South Asian 1.8%; Americas 3.8%; Ashkenazi 2.9%; Finnish 1.2%; Middle Eastern 6.1%; Amish 7.2%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Cardiovascular & Metabolic
Diabetes & Glycemic Traits
Type 2 Diabetes. Evidence: 5/10. Source: PMID 17977958. Lower Risk.
Fasting Glucose. Evidence: 10/10. Source: PMID 31217584. Typical.
HbA1c. Evidence: 10/10. Source: PMID 20858683. Typical.
Metabolic Syndrome & Insulin Resistance
Metabolic Syndrome. Evidence: 6/10. Source: PMID 38201907. Typical Risk.
Endocrine & Reproductive
Pregnancy & Birth Complications
Birth Weight. Evidence: 3/10. Source: PMID 20682688. Typical.
Showing effects for C/T genotype
Type 2 Diabetes. Evidence: 5/10. Source: PMID 17977958. ~1.3x Increased Risk.
Fasting Glucose. Evidence: 10/10. Source: PMID 31217584. Slightly Elevated.
HbA1c. Evidence: 10/10. Source: PMID 20858683. Slightly Elevated.
Metabolic Syndrome. Evidence: 6/10. Source: PMID 38201907. Slightly Higher Risk.
Birth Weight. Evidence: 3/10. Source: PMID 20682688. ~27g Heavier.
Showing effects for T/T genotype
Type 2 Diabetes. Evidence: 5/10. Source: PMID 17977958. ~2.7x Increased Risk.
Fasting Glucose. Evidence: 10/10. Source: PMID 31217584. Elevated.
HbA1c. Evidence: 10/10. Source: PMID 20858683. Elevated.
Metabolic Syndrome. Evidence: 6/10. Source: PMID 38201907. Higher Risk.
Birth Weight. Evidence: 3/10. Source: PMID 20682688. ~54g Heavier.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Fasting blood glucose levels remain at a typical baseline because glucokinase expression in the pancreas is fully functional [1]. This optimal enzyme activity ensures that insulin is released efficiently when blood sugar rises, maintaining metabolic stability [1]. Large-scale genomic studies show that having two copies of the C allele is associated with a lower risk of developing type 2 diabetes [2]. During pregnancy, maternal blood glucose levels are kept in a healthy range, resulting in typical infant birth weights [3]. Long-term tracking indicates stable glycated hemoglobin (HbA1c) levels over time [4]. This genotype represents the standard metabolic baseline found in the majority of the global population.
Typical fasting blood glucose levels; Lower risk of type 2 diabetes; Typical infant birth weight.
Sample genotype: CT (Heterozygous)
Fasting blood glucose levels are slightly elevated due to a minor reduction in glucokinase promoter activity in pancreatic cells [1]. This change raises the threshold required to trigger insulin secretion, leading to a subtle but persistent increase in circulating glucose [2]. Prospective clinical studies indicate that carrying one copy of the T allele increases the risk of type 2 diabetes by approximately 1.3-fold [3]. Pregnant mothers with this genotype tend to have slightly higher blood sugar, which can lead to babies being born about 27 grams heavier on average [4]. Glycated hemoglobin (HbA1c) levels are also marginally higher compared to the baseline genotype [5]. Managing diet and maintaining physical activity can help mitigate these subtle metabolic shifts.
Slightly elevated fasting glucose; 1.3x increased risk of type 2 diabetes; Slightly higher infant birth weight.
Sample genotype: TT (Homozygous)
Fasting blood glucose levels are consistently higher because glucokinase promoter activity is significantly reduced in pancreatic beta-cells [1]. This reduction shifts the glucose-sensing threshold upward, requiring higher blood sugar levels to stimulate insulin release [2]. Clinical studies show that having two copies of the T allele is associated with an estimated 2.7-fold increased risk of type 2 diabetes [3]. Pregnant mothers with this genotype have elevated blood glucose, which often results in babies being born about 54 grams heavier due to increased fetal insulin production [4]. Glycated hemoglobin (HbA1c) levels are also notably higher, reflecting long-term elevated blood sugar [5]. Proactive metabolic monitoring and lifestyle interventions are highly beneficial for managing these genetic tendencies.
Elevated fasting glucose levels; 2.7x increased risk of type 2 diabetes; Higher infant birth weight.
Variants with shared genetic architecture
rs4607517 · GCK Gene · Chr 7 · Type 2 Diabetes Risk
rs2070971 · GCK Gene · Chr 7 · Blood Triglycerides
rs730497 · GCK Gene · Chr 7 · Blood Sugar and Diabetes
Monogenic models: what have the single gene disorders taught us?
Common variants in maturity-onset diabetes of the young genes and future risk of type 2 diabetes.
[Fasting hyperglycaemia and polymorphism in glucokinase promoter (rs1799884)].
Impact of common type 2 diabetes risk polymorphisms in the DESIR prospective study.
Content updated August 2026.
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