What you carry at this position in your DNA and what research says about it.
Type 2 Diabetes Risk: 10/10 evidence, 37 publications.
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Sample genotype (not yours): A/A
Higher Risk of Type 2 Diabetes
Carrying two copies of the A allele is linked to reduced ADCY5 expression in the pancreas, which can impair insulin secretion. This genotype is associated with higher fasting blood sugar, elevated HbA1c, and an increased likelihood of developing type 2 diabetes.
What this genotype means: Reduced pancreatic ADCY5 expression; Impaired glucose-stimulated insulin secretion; Elevated fasting blood sugar and HbA1c.
Sample genotype (not yours): A/G
Moderately Higher Risk of Type 2 Diabetes
Carrying one copy of the A allele is associated with a moderate reduction in pancreatic ADCY5 expression. This can lead to slightly elevated fasting blood sugar levels and a modest increase in type 2 diabetes risk.
What this genotype means: Mildly reduced pancreatic ADCY5 expression; Slightly blunted insulin response to glucose; Modestly elevated fasting blood sugar.
Sample genotype (not yours): G/G
Typical Risk of Type 2 Diabetes
Carrying two copies of the G allele supports typical ADCY5 expression in the pancreas, promoting efficient insulin release. This genotype is associated with lower fasting blood sugar levels and a typical risk of type 2 diabetes.
What this genotype means: Preserved pancreatic ADCY5 expression; Efficient insulin secretion in response to glucose; Typical fasting blood sugar and HbA1c.
Gene function and biological role
Gene Function: The ADCY5 gene encodes adenylate cyclase 5, an enzyme responsible for catalyzing the conversion of adenosine triphosphate into cyclic adenosine monophosphate [1]. In pancreatic beta-cells, this cyclic nucleotide acts as a vital second messenger that couples glucose sensing to the physical release of insulin [1]. Proper expression of this gene is essential for maintaining glucose homeostasis and preventing chronic elevations in blood sugar [1]. Beyond the pancreas, ADCY5 is expressed in adipose and cardiovascular tissues, where it influences lipid metabolism and cellular energy pathways [2].
Variant Impact: The rs11708067 variant is located within an intron of the ADCY5 gene and overlaps a critical regulatory enhancer region in pancreatic islets [3]. The A allele at this position disrupts the enhancer's activity, leading to reduced transcription of the ADCY5 gene and lower enzyme levels in the pancreas [3]. This reduction in expression impairs glucose-stimulated insulin secretion, making it harder for the body to manage sudden increases in blood sugar [3]. Consequently, this single-nucleotide change is a major genetic determinant of fasting glucose levels and susceptibility to metabolic conditions [4].
Key Insight: This variant affects blood sugar levels by directly weakening the genetic enhancer that controls insulin release in the pancreas, rather than by causing insulin resistance in muscle or fat tissues.
Location: ADCY5. Chromosome 3 · 3q21.1 · 123.3 Mb
Estimated prevalence by population
Global 65.4%; European 60.1%; African 72.1%; East Asian 99.5%; South Asian 64.2%; Americas 54.6%; Ashkenazi 69.9%; Finnish 70.4%; Middle Eastern 69.4%; Amish 66.7%.
Estimated AA genotype frequency.
Global 30.6%; European 34.8%; African 25.6%; East Asian 0.5%; South Asian 31.8%; Americas 38.6%; Ashkenazi 27.4%; Finnish 27.0%; Middle Eastern 27.8%; Amish 29.9%.
Estimated AG genotype frequency.
Global 4.0%; European 5.0%; African 2.3%; East Asian < 0.1%; South Asian 3.9%; Americas 6.8%; Ashkenazi 2.7%; Finnish 2.6%; Middle Eastern 2.8%; Amish 3.4%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Cardiovascular & Metabolic
Diabetes & Glycemic Traits
Type 2 Diabetes. Evidence: 10/10. Source: PMID 32541925. ~1.2x Higher Risk.
Fasting Glucose. Evidence: 10/10. Source: PMID 20081858. Elevated Glucose.
HbA1c. Evidence: 9/10. Source: PMID 28898252. Higher HbA1c.
Beta-Cell Function. Evidence: 8/10. Source: PMID 20081858. Lower Function.
Lipids & Cholesterol
Total Cholesterol. Evidence: 8/10. Source: PMID 29083408. Slightly Higher.
Endocrine & Reproductive
Pregnancy & Birth Complications
Birth Weight. Evidence: 8/10. Source: PMID 20490451. Lower Birth Weight.
Showing effects for A/G genotype
Type 2 Diabetes. Evidence: 10/10. Source: PMID 32541925. ~1.1x Higher Risk.
Fasting Glucose. Evidence: 10/10. Source: PMID 20081858. Slightly Elevated.
HbA1c. Evidence: 9/10. Source: PMID 28898252. Slightly Higher.
Beta-Cell Function. Evidence: 8/10. Source: PMID 20081858. Slightly Lower.
Total Cholesterol. Evidence: 8/10. Source: PMID 29083408. Typical.
Birth Weight. Evidence: 8/10. Source: PMID 20490451. Slightly Lower.
Showing effects for G/G genotype
Type 2 Diabetes. Evidence: 10/10. Source: PMID 32541925. Typical Risk.
Fasting Glucose. Evidence: 10/10. Source: PMID 20081858. Typical Glucose.
HbA1c. Evidence: 9/10. Source: PMID 28898252. Typical HbA1c.
Beta-Cell Function. Evidence: 8/10. Source: PMID 20081858. Typical Function.
Total Cholesterol. Evidence: 8/10. Source: PMID 29083408. Slightly Lower.
Birth Weight. Evidence: 8/10. Source: PMID 20490451. Typical Birth Weight.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Pancreatic beta-cells rely on ADCY5 to translate glucose signals into insulin release, a process that is less efficient with this genotype [1]. Studies show that carrying two copies of the A allele significantly lowers ADCY5 expression in islet cells, leading to a blunted insulin response when blood sugar rises [1]. This impairment is reflected in elevated fasting glucose levels and higher HbA1c, which are key markers of long-term glycemic control [2]. Large-scale genomic analyses consistently link this genotype to an increased risk of type 2 diabetes [3]. Additionally, because fetal insulin is a primary driver of prenatal growth, this genotype is associated with slightly lower average birth weight [4]. It is also linked to slightly higher total cholesterol levels, though its primary impact remains centered on glucose metabolism [5].
Reduced pancreatic ADCY5 expression; Impaired glucose-stimulated insulin secretion; Elevated fasting blood sugar and HbA1c; Increased susceptibility to type 2 diabetes.
Sample genotype: AG (Heterozygous)
Having one copy of the A allele and one copy of the G allele represents an intermediate state for pancreatic ADCY5 expression and insulin secretion [1]. The presence of the A allele partially disrupts the pancreatic islet enhancer, leading to a mild reduction in the insulin response to glucose [1]. Clinical studies indicate that this intermediate expression level translates to a modest elevation in fasting blood sugar and HbA1c compared to the protective genotype [2]. The risk of developing type 2 diabetes is slightly increased, though not as pronounced as in those with two copies of the risk allele [3]. Fetal growth may also be slightly affected, resulting in a minor reduction in birth weight due to lower prenatal insulin levels [4]. Lipid profiles show a very slight trend toward higher total cholesterol, while inflammatory markers like C-reactive protein remain near typical levels [5].
Mildly reduced pancreatic ADCY5 expression; Slightly blunted insulin response to glucose; Modestly elevated fasting blood sugar; Slightly increased risk of type 2 diabetes.
Sample genotype: GG (Homozygous)
Pancreatic beta-cells function optimally when ADCY5 expression is fully maintained, which is supported by carrying two copies of the G allele [1]. This genotype preserves the integrity of the islet enhancer, allowing for robust insulin secretion in response to glucose [1]. Consequently, individuals with this genetic profile tend to have lower fasting blood sugar and more stable HbA1c levels [2]. Large-scale association studies confirm that this genotype is protective against type 2 diabetes, representing the baseline risk level [3]. During fetal development, typical insulin secretion supports healthy prenatal growth, which is associated with standard birth weights [4]. While this genotype is linked to slightly lower total cholesterol, it is also associated with slightly higher levels of C-reactive protein, though this minor inflammatory marker change does not outweigh the metabolic benefits [5].
Preserved pancreatic ADCY5 expression; Efficient insulin secretion in response to glucose; Typical fasting blood sugar and HbA1c; Standard baseline risk of type 2 diabetes.
Variants with shared genetic architecture
rs2877716 · ADCY5 Gene · Chr 3 · Type 2 Diabetes Risk
rs11257655 · CDC123 Gene · Chr 10 · Type 2 Diabetes Risk
rs4402960 · IGF2BP2 Gene · Chr 3 · Type 2 Diabetes Risk
Glucose-raising genetic variants in MADD and ADCY5 impair conversion of proinsulin to insulin.
ADCY5 gene expression in adipose tissue is related to obesity in men and mice.
New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.
The power of genetic diversity in genome-wide association studies of lipids.
A cross-population atlas of genetic associations for 220 human phenotypes.
Content updated August 2026.
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