What you carry at this position in your DNA and what research says about it.
Type 2 Diabetes Risk: 10/10 evidence, 18 publications.
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Sample genotype (not yours): T/T
Lower Risk of Type 2 Diabetes
Fasting blood sugar levels tend to remain in the typical, healthy range. Pancreatic beta cells maintain optimal insulin secretion, and there is no elevated risk of blood sugar spikes from beta-blocker medications.
What this genotype means: Optimal pancreatic beta-cell function; Lower risk of type 2 diabetes; Stable blood sugar on beta-blocker therapy.
Sample genotype (not yours): C/C
Higher Risk of Type 2 Diabetes
Fasting blood sugar levels are typically elevated due to reduced pancreatic insulin secretion. There is a pronounced risk of blood sugar spikes when treated with the beta-blocker atenolol.
What this genotype means: Reduced pancreatic insulin secretion; Elevated fasting blood glucose levels; Pronounced blood sugar rise on atenolol.
Sample genotype (not yours): T/C
Slightly Higher Risk of Type 2 Diabetes
Fasting blood sugar levels may be slightly elevated due to a mild reduction in pancreatic insulin secretion. Taking the blood pressure medication atenolol can trigger a modest increase in blood sugar.
What this genotype means: Mildly reduced insulin secretion capacity; Slightly elevated fasting blood glucose; Modest blood sugar rise on atenolol.
Gene function and biological role
Gene Function: The PROX1 gene encodes prospero homeobox 1, a transcription factor essential for the embryonic development of the pancreas, liver, and lymphatic system [1]. In the pancreas, this protein plays a critical role in the formation and maturation of insulin-producing beta cells [1]. Research indicates that reduced expression of this gene impairs glucose-stimulated insulin secretion, directly impacting systemic glucose tolerance [1]. Beyond pancreatic development, it regulates metabolic pathways in the liver, including gluconeogenesis and lipid metabolism [2]. Consequently, genetic variations that alter its expression levels are strongly linked to metabolic disorders and glycemic control [2].
Variant Impact: The rs340874 variant is an intronic single-nucleotide polymorphism located in the 5 prime region of the PROX1 gene [1]. This genetic change acts as a cis-regulatory element that modulates the transcriptional activity and expression levels of the gene [1]. Studies in pancreatic cells show that the risk-associated allele alters nuclear protein binding, leading to reduced gene expression and impaired insulin secretion [1]. Large-scale genome-wide association studies have firmly established this variant as a key genetic determinant of fasting blood glucose levels and type 2 diabetes susceptibility [2]. Additionally, it influences how blood sugar levels respond to certain common blood pressure medications [3].
Key Insight: This variant not only predisposes individuals to higher fasting blood sugar but also predicts an exaggerated blood sugar spike when taking the common blood pressure medication atenolol.
Location: PROX1. Chromosome 1 · 1q32.3 · 214.0 Mb
Estimated prevalence by population
Global 37.4%; European 20.8%; African 69.6%; East Asian 36.3%; South Asian 22.1%; Americas 34.1%; Ashkenazi 28.5%; Finnish 35.2%; Middle Eastern 32.3%; Amish 15.2%.
Estimated TT genotype frequency.
Global 43.3%; European 49.6%; African 27.7%; East Asian 47.9%; South Asian 49.8%; Americas 48.6%; Ashkenazi 49.8%; Finnish 48.3%; Middle Eastern 49.1%; Amish 47.6%.
Estimated TC genotype frequency.
Global 19.3%; European 29.6%; African 2.8%; East Asian 15.8%; South Asian 28.1%; Americas 17.3%; Ashkenazi 21.7%; Finnish 16.6%; Middle Eastern 18.7%; Amish 37.3%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Cardiovascular & Metabolic
Diabetes & Glycemic Traits
Type 2 Diabetes. Evidence: 10/10. Source: PMID 20081858. Lower Risk.
Fasting Glucose. Evidence: 8/10. Source: PMID 20081858. Typical Levels.
Beta-Cell Function. Evidence: 7/10. Source: PMID 20081858. Optimal Function.
Diabetic Complications. Evidence: 6/10. Source: PMID 39024449. Lower Risk.
Pharmacogenomics
Cardiovascular Drug Response
Atenolol Blood Sugar Effect. Evidence: 5/10. Source: PMID 24122840. No Elevation.
Showing effects for C/C genotype
Type 2 Diabetes. Evidence: 10/10. Source: PMID 20081858. Higher Risk.
Fasting Glucose. Evidence: 8/10. Source: PMID 20081858. Elevated Levels.
Beta-Cell Function. Evidence: 7/10. Source: PMID 20081858. Reduced Function.
Diabetic Complications. Evidence: 6/10. Source: PMID 39024449. Higher Risk.
Atenolol Blood Sugar Effect. Evidence: 5/10. Source: PMID 24122840. Pronounced Elevation.
Showing effects for T/C genotype
Type 2 Diabetes. Evidence: 10/10. Source: PMID 20081858. Slightly Higher Risk.
Fasting Glucose. Evidence: 8/10. Source: PMID 20081858. Slightly Elevated.
Beta-Cell Function. Evidence: 7/10. Source: PMID 20081858. Slightly Reduced.
Diabetic Complications. Evidence: 6/10. Source: PMID 39024449. Slightly Higher Risk.
Atenolol Blood Sugar Effect. Evidence: 5/10. Source: PMID 24122840. Modest Elevation.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Pancreatic beta cells function at their optimal capacity to secrete insulin in response to glucose fluctuations [1]. Having two copies of the protective T allele is associated with lower fasting blood glucose levels and a decreased risk of developing type 2 diabetes [1]. Large-scale clinical trials show that individuals with this genotype do not experience the adverse blood sugar elevations typically triggered by the beta-blocker atenolol [2]. In fact, blood sugar levels may even slightly decrease during treatment with this medication [2]. The protective nature of this genotype extends to a lower baseline risk for diabetic complications such as neuropathy and retinopathy [3]. Maintaining a balanced diet and regular physical activity further supports this favorable genetic baseline. Overall, this genetic profile represents the most metabolic-friendly combination at this locus.
Optimal pancreatic beta-cell function; Lower risk of type 2 diabetes; Stable blood sugar on beta-blocker therapy.
Sample genotype: CC (Homozygous)
Pancreatic beta cells experience a significant reduction in their ability to secrete insulin in response to glucose [1]. Carrying two copies of the C allele is strongly associated with elevated fasting blood glucose and a higher risk of developing type 2 diabetes [2]. This genetic profile also correlates with a higher accumulation of visceral fat and altered postprandial lipid metabolism [3]. In clinical settings, individuals with this genotype show a pronounced susceptibility to beta-blocker-induced hyperglycemia [4]. Furthermore, this genotype is linked to an increased risk of diabetic complications, including neuropathy and retinopathy [5].
Reduced pancreatic insulin secretion; Elevated fasting blood glucose levels; Pronounced blood sugar rise on atenolol.
Sample genotype: TC (Heterozygous)
Pancreatic beta cells exhibit a mild reduction in their capacity to secrete insulin efficiently [1]. Carrying one copy of the risk-associated C allele is linked to a slight increase in fasting blood glucose levels and a moderately elevated risk of type 2 diabetes [2]. Clinical studies demonstrate that this genotype is susceptible to medication-induced hyperglycemia [3]. This subtle metabolic shift highlights the importance of monitoring glycemic markers when undergoing antihypertensive therapy. There is also a slightly higher predisposition to diabetic microvascular complications like neuropathy and retinopathy over time [4]. Adopting proactive lifestyle habits, such as a low-glycemic diet, can help counteract this genetic tendency. Healthcare providers often consider these genetic factors when choosing the most appropriate blood pressure medications.
Mildly reduced insulin secretion capacity; Slightly elevated fasting blood glucose; Modest blood sugar rise on atenolol.
Variants with shared genetic architecture
rs10830963 · MTNR1B Gene · Chr 11 · Type 2 Diabetes Risk
rs11257655 · CDC123 Gene · Chr 10 · Type 2 Diabetes Risk
rs11558471 · SLC30A8 Gene · Chr 8 · Type 2 Diabetes Risk
Genetic and molecular insights into the role of PROX1 in glucose metabolism.
New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.
PROX1 gene variant is associated with fasting glucose change after antihypertensive treatment.
Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
Content updated August 2026.
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