What you carry at this position in your DNA and what research says about it.
Type 2 Diabetes Risk: 10/10 evidence, 59 publications.
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Sample genotype (not yours): G/G
Typical Insulin Secretion and Diabetes Risk
Optimal pancreatic beta-cell function supports normal insulin release after meals. This genotype is associated with typical blood sugar levels and a standard risk of metabolic conditions.
What this genotype means: Typical insulin secretion after meals; Standard baseline risk for type 2 diabetes; Typical blood pressure regulation.
Sample genotype (not yours): C/C
Increased Risk of Type 2 Diabetes
Two copies of the C allele are linked to lower insulin secretion after meals. This can lead to higher post-meal blood sugar spikes and an increased risk of diabetes.
What this genotype means: Reduced insulin secretion following meals; Elevated risk for type 2 diabetes; Better response to DPP-4 inhibitor medications.
Sample genotype (not yours): G/C
Slightly Increased Risk of Type 2 Diabetes
A single copy of the C allele is linked to slightly lower insulin secretion after meals. This can lead to higher post-meal blood sugar spikes and a modest increase in diabetes risk.
What this genotype means: Slightly reduced insulin release after meals; Modestly increased risk for type 2 diabetes; Slightly higher susceptibility to gestational diabetes.
Gene function and biological role
Gene Function: The CDKAL1 gene encodes a protein that is highly active in the insulin-producing beta cells of the pancreas [1]. It plays a critical role in modifying transfer RNA, which is essential for the precise translation and folding of proinsulin. When this gene functions optimally, pancreatic beta cells can efficiently sense rising blood glucose levels and release insulin to maintain metabolic balance [1]. Disruptions or variations in this gene can impair insulin secretion, leading to chronic elevations in blood sugar [2]. Over time, this cellular strain can contribute to the development of metabolic disorders [2].
Variant Impact: The rs7754840 variant is located within an intron of the CDKAL1 gene and is one of the most widely replicated genetic markers for metabolic health [3]. The change from a G allele to a C allele alters the regulation of the gene, leading to reduced insulin secretion in response to glucose [3]. This reduction in first-phase insulin release makes it more difficult for the body to clear blood sugar spikes after meals [3]. Consequently, this variant is strongly associated with elevated blood glucose, higher HbA1c levels, and an increased susceptibility to type 2 diabetes [2].
Key Insight: While the C allele increases the risk of developing type 2 diabetes, individuals with the C/C genotype actually show a significantly better therapeutic response to DPP-4 inhibitor medications.
Location: CDKAL1. Chromosome 6 · 6p22.3 · 20.7 Mb
Estimated prevalence by population
Global 37.8%; European 46.9%; African 17.4%; East Asian 37.4%; South Asian 53.8%; Americas 45.6%; Ashkenazi 42.8%; Finnish 39.3%; Middle Eastern 44.0%; Amish 38.8%.
Estimated GG genotype frequency.
Global 45.1%; European 43.2%; African 48.6%; East Asian 47.5%; South Asian 39.1%; Americas 43.9%; Ashkenazi 45.2%; Finnish 46.8%; Middle Eastern 44.7%; Amish 47.0%.
Estimated GC genotype frequency.
Global 17.1%; European 9.9%; African 34.0%; East Asian 15.1%; South Asian 7.1%; Americas 10.6%; Ashkenazi 11.9%; Finnish 13.9%; Middle Eastern 11.3%; Amish 14.2%.
Estimated CC genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Diabetes & Glycemic Traits
Type 2 Diabetes. Evidence: 10/10. Source: PMID 17463246. Typical Risk.
Blood Glucose. Evidence: 4/10. Source: PMID 31902109. Typical.
Hypertension
Blood Pressure. Evidence: 6/10. Source: PMID 33230300. Typical.
Endocrine & Reproductive
Pregnancy & Birth Complications
Gestational Diabetes. Evidence: 5/10. Source: PMID 22233651. Typical Risk.
Pharmacogenomics
Diabetes Medication Response
DPP-4 Inhibitor Response. Evidence: 5/10. Source: PMID 27139004. Typical Response.
Showing effects for C/C genotype
Type 2 Diabetes. Evidence: 10/10. Source: PMID 17463246. ~1.3x Increased Risk.
Blood Glucose. Evidence: 4/10. Source: PMID 31902109. Slightly Elevated.
Blood Pressure. Evidence: 6/10. Source: PMID 33230300. Slightly Elevated.
Gestational Diabetes. Evidence: 5/10. Source: PMID 22233651. ~1.5x Increased Risk.
DPP-4 Inhibitor Response. Evidence: 5/10. Source: PMID 27139004. Stronger Response.
Showing effects for G/C genotype
Gestational Diabetes. Evidence: 5/10. Source: PMID 22233651. Increased Risk.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Pancreatic beta cells function at their baseline capacity, allowing for efficient first-phase insulin release when blood sugar rises [1]. This prompt response helps clear glucose from the bloodstream quickly after eating, preventing prolonged blood sugar spikes [1]. Because insulin secretion is unimpeded, there is no genetically elevated risk for type 2 diabetes or gestational diabetes associated with this locus [2]. Blood pressure and overall cardiovascular markers also tend to remain within typical ranges [3]. Maintaining a balanced diet and regular physical activity will continue to support this natural metabolic efficiency. This genotype represents the most common baseline in many populations, serving as a standard reference for metabolic health.
Typical insulin secretion after meals; Standard baseline risk for type 2 diabetes; Typical blood pressure regulation.
Sample genotype: CC (Homozygous)
Carrying two copies of the risk allele is associated with a more pronounced reduction in first-phase insulin release from pancreatic beta cells [1]. This significant delay in insulin secretion means that blood sugar levels can remain elevated for longer periods after meals [1]. Over time, this metabolic strain increases the risk of developing type 2 diabetes by approximately thirty percent [2]. It is also associated with a higher likelihood of gestational diabetes during pregnancy [3]. Additionally, subtle increases in blood pressure and HbA1c levels have been observed in individuals with this genotype [4]. Interestingly, individuals with this genotype may show a better therapeutic response to DPP-4 inhibitor medications if they require treatment for diabetes [5]. Proactive lifestyle choices, such as prioritizing high-fiber foods and regular exercise, can effectively offset this genetic predisposition.
Reduced insulin secretion following meals; Elevated risk for type 2 diabetes; Better response to DPP-4 inhibitor medications.
Sample genotype: GC (Heterozygous)
Carrying one copy of the risk allele is associated with a measurable reduction in first-phase insulin release from pancreatic beta cells [1]. This slight delay in insulin secretion means that blood sugar levels may take longer to return to baseline after eating [1]. Over time, this mild metabolic strain increases the risk of developing type 2 diabetes by about thirty percent [2]. It is also associated with a higher likelihood of gestational diabetes during pregnancy [3]. Additionally, subtle increases in blood pressure and HbA1c levels have been observed in individuals with this genotype [4]. Proactive lifestyle choices, such as prioritizing high-fiber foods and regular exercise, can effectively offset this genetic predisposition. This genotype represents a very common metabolic profile that responds well to standard healthy habits.
Slightly reduced insulin release after meals; Modestly increased risk for type 2 diabetes; Slightly higher susceptibility to gestational diabetes.
Variants with shared genetic architecture
rs7756992 · CDKAL1 Gene · Chr 6 · Type 2 Diabetes Risk
rs9368222 · CDKAL1 Gene · Chr 6 · Type 2 Diabetes Risk
rs10440833 · CDKAL1 Gene · Chr 6 · Type 2 Diabetes Risk
The risk allele load accelerates the age-dependent decline in beta cell function.
A genome-wide association study of gestational diabetes mellitus in Korean women.
Content updated August 2026.
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