What you carry at this position in your DNA and what research says about it.
Metabolic Syndrome Risk: 7/10 evidence, 33 publications.
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Sample genotype (not yours): G/G
Lower Metabolic Syndrome and Glucose Risk
Carrying two G alleles is associated with lower fasting glucose, lower triglycerides, and a reduced risk of metabolic syndrome. It also links to slightly higher LDL and total cholesterol levels.
What this genotype means: Lower risk of metabolic syndrome; Lower fasting blood glucose; Slightly higher LDL cholesterol.
Sample genotype (not yours): A/A
Higher Metabolic Syndrome and Glucose Risk
Carrying two A alleles is associated with higher fasting glucose, elevated triglycerides, and an increased risk of metabolic syndrome. Conversely, it links to lower LDL and total cholesterol levels.
What this genotype means: Higher risk of metabolic syndrome; Elevated fasting blood glucose; Lower LDL cholesterol.
Sample genotype (not yours): A/G
Typical Metabolic Profile
An intermediate genetic profile balances a slight increase in glucose and triglycerides with a slight reduction in LDL cholesterol. Most metabolic markers remain near the population average.
What this genotype means: Typical metabolic syndrome risk; Average fasting blood glucose; Typical cholesterol levels.
Gene function and biological role
Gene Function: The LOC157273 gene is a long non-coding RNA transcript located on chromosome 8 [1]. Although it does not code for a protein itself, it acts as a crucial transcriptional repressor for the nearby PPP1R3B gene [1]. The PPP1R3B gene encodes a regulatory subunit of protein phosphatase 1, which is a key enzyme that controls glycogen synthesis in the liver [1]. By regulating glycogen storage, this pathway plays a major role in maintaining whole-body glucose and energy homeostasis [1]. Alterations in this regulatory network can shift the liver's energy storage balance between lipids and glycogen, directly impacting circulating cholesterol and triglyceride levels [2].
Variant Impact: The rs9987289 variant is an intronic change located within the LOC157273 gene region [1]. This genetic variant functions as a liver expression quantitative trait locus that modulates the expression of the nearby PPP1R3B gene [1]. The minor A allele of this variant is associated with decreased levels of the LOC157273 repressor, which subsequently increases PPP1R3B expression in liver tissue [1]. This shift in gene expression enhances hepatic glycogen storage but alters systemic lipid and glucose metabolism [1]. Consequently, this single nucleotide change has been robustly linked to variations in blood lipids, fasting glucose, and markers of systemic inflammation [2].
Key Insight: This variant acts as a genetic switch in the liver, shifting energy storage from fats to glycogen.
Location: PPP1R3B. Chromosome 8 · 8p23.1 · 9.3 Mb
Estimated prevalence by population
Global 1.8%; European 0.8%; African 3.5%; East Asian < 0.1%; South Asian 1.2%; Americas 2.9%; Ashkenazi 0.3%; Finnish 2.6%; Middle Eastern 0.5%; Amish < 0.1%.
Estimated AA genotype frequency.
Global 21.4%; European 15.9%; African 30.5%; East Asian 2.4%; South Asian 19.3%; Americas 28.4%; Ashkenazi 10.7%; Finnish 27.2%; Middle Eastern 13.3%; Amish 0.7%.
Estimated AG genotype frequency.
Global 76.7%; European 83.3%; African 66.0%; East Asian 97.6%; South Asian 79.5%; Americas 68.7%; Ashkenazi 89.0%; Finnish 70.1%; Middle Eastern 86.2%; Amish 99.3%.
Estimated GG genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
LDL Cholesterol. Evidence: 10/10.
Triglycerides. Evidence: 8/10. Source: PMID 21386085. Typical.
Diabetes & Glycemic Traits
Blood Glucose. Evidence: 10/10. Source: PMID 34059833. Typical.
Metabolic Syndrome & Insulin Resistance
Metabolic Syndrome. Evidence: 7/10. Source: PMID 21386085. Lower Risk.
Immunity & Inflammation
Inflammatory & Circulating Protein Markers
Inflammation. Evidence: 8/10. Source: PMID 21300955. Typical.
Showing effects for A/A genotype
LDL Cholesterol. Evidence: 10/10. Source: PMID 20686565. Typical.
Triglycerides. Evidence: 8/10. Source: PMID 21386085. Higher.
Blood Glucose. Evidence: 10/10. Source: PMID 34059833. Higher.
Metabolic Syndrome. Evidence: 7/10. Source: PMID 21386085. Higher Risk.
Inflammation. Evidence: 8/10. Source: PMID 21300955. Higher.
Showing effects for A/G genotype
Triglycerides. Evidence: 8/10. Source: PMID 21386085. Slightly Higher.
Blood Glucose. Evidence: 10/10. Source: PMID 34059833. Slightly Higher.
Metabolic Syndrome. Evidence: 7/10. Source: PMID 21386085. Typical Risk.
Inflammation. Evidence: 8/10. Source: PMID 21300955. Slightly Higher.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
A double G profile represents the most common genetic makeup globally. Large-scale genome-wide association studies show that this genetic signature is linked to lower fasting blood glucose levels and a reduced risk of developing metabolic syndrome [1]. It also associates with lower circulating triglycerides and reduced markers of systemic inflammation, such as C-reactive protein [2]. These metabolic benefits are driven by lower expression of the hepatic PPP1R3B gene, which coordinates glycogen storage in the liver [3]. On the other hand, this profile is associated with slightly higher levels of LDL and total cholesterol [4]. Overall, this profile represents a favorable metabolic balance with lower risk for insulin resistance and related disorders.
Lower risk of metabolic syndrome; Lower fasting blood glucose; Slightly higher LDL cholesterol.
Sample genotype: AA (Homozygous)
A double A profile is associated with a distinct metabolic signature characterized by higher fasting blood glucose and insulin levels [1]. This genetic variation significantly increases the risk of developing metabolic syndrome, a cluster of conditions that raise the risk of heart disease and type 2 diabetes [1]. It also links to elevated circulating triglycerides and higher levels of C-reactive protein, a marker of systemic inflammation [2]. These effects are mediated by increased expression of the PPP1R3B gene in the liver, which enhances glycogen storage at the expense of other metabolic pathways [3]. Interestingly, this profile is associated with lower levels of LDL and total cholesterol, which is typically considered protective [4]. However, the elevated glucose, triglycerides, and inflammatory markers generally outweigh the benefit of lower LDL cholesterol. Maintaining a balanced diet and regular physical activity is particularly beneficial for individuals with this genetic profile to support metabolic health.
Higher risk of metabolic syndrome; Elevated fasting blood glucose; Lower LDL cholesterol.
Sample genotype: AG (Heterozygous)
Possessing one copy of each allele results in a balanced metabolic profile. This intermediate state is associated with typical levels of fasting blood glucose and average risk for metabolic syndrome [1]. Circulating triglycerides and inflammatory markers like C-reactive protein are generally within the normal range [2]. The presence of one G allele keeps hepatic PPP1R3B expression at moderate levels, maintaining a standard balance of glycogen storage [3]. Additionally, this profile exhibits slightly lower LDL and total cholesterol levels compared to the G/G genotype, offsetting the minor metabolic risks [4]. Most individuals with this genetic makeup do not experience significant deviations from baseline metabolic health due to this variant alone. Standard healthy lifestyle choices remain the primary driver of cardiovascular and metabolic outcomes.
Typical metabolic syndrome risk; Average fasting blood glucose; Typical cholesterol levels.
Variants with shared genetic architecture
rs4240624 · PPP1R3B Gene · Chr 8 · Gallstone and Cholesterol Risk
rs4841132 · PPP1R3B Gene · Chr 8 · Metabolic Trade-Off
rs2126259 · PPP1R3B Gene · Chr 8 · Metabolic Health Balance
Genome-Wide Association Study of the Metabolic Syndrome in UK Biobank.
Biological, clinical and population relevance of 95 loci for blood lipids.
Content updated August 2026.
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