ArticleDiabetology & metabolic syndrome2024
The impact of sex hormones on metabolic syndrome: univariable and multivariable Mendelian randomization studies.
Article in Diabetology & metabolic syndrome, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Article
- Exposure to per- and polyfluoroalkyl substances and adult cardiometabolic health: a Canadian Health Measures Survey mixture analysis.Environmental health : a global access science source · 2026Article
- Testosterone-related indices and adverse glucose-lipid metabolic status in men: a single-center retrospective study.Frontiers in endocrinology · 2026Article
- Sex-specific Mendelian randomization phenome-wide association study of basal metabolic rate.Scientific reports · 2025Article
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Abstract
backgroundObservational studies have found associations between sex hormones and metabolic syndrome(Mets), but the causal relationships remains unclear. This study utilizes univariable and multivariable Mendelian randomization (MR) to elucidate the associations between sex hormones (including sex hormone-binding globulin(SHBG), estradiol(E2), testosterone(T)) and Mets and its subtypes (including waist circumference(WC), fasting blood glucose(FBG), high blood pressure(HBP), high-density lipoprotein(HDL-C), triglycerides(TG)).
methodsWe utilized summary data from large-scale genome-wide association studies. Univariable Mendelian randomization (UMVMR) analysis was primarily conducted using the inverse variance weighted method (IVW), with secondary analyses employing the weighted median, MR-Egger regression, simple mode method, and weighted mode method. Subsequently, multivariable Mendelian randomization (MVMR) was employed to assess the causal relationships between SHBG, T, E2, and MetS and its components: WC, FPG, HBP, HDL-C, and TG. Sensitivity analyses were conducted to assess result reliability.
resultsGenetically predicted SHBG was significantly negatively associated with MetS (UMVMR: β=-0.72; 95% CI = 0.41 to 0.57; P = 1.28e-17; MVMR: β=-0.60; 95% CI=-0.83 to -0.38; P < 0.001). Positive causal relationships were observed between SHBG and WC(MVMR: β = 0.10; 95% CI = 0.03 to 0.17; P = 0.01) and HDL-C (MVMR: β = 0.41; 95% CI = 0.21 to 0.60; P < 0.001), while negative causal relationships were found between SHBG and HBP (MVMR: β=-0.02; 95% CI=-0.04 to -0.00; P = 0.02), TG (MVMR: β=-0.48; 95% CI=-0.70 to -0.26; P < 0.001). Genetically predicted E2 exhibited a negative association with TG (MVMR: β=-1.49; 95% CI=-2.48 to -0.50; P = 0.003). Genetically predicted T was negatively associated with TG (MVMR: β=-0.36; 95% CI=-0.71 to -0.00; P = 0.049) and WC (MVMR: β=-0.13; 95% CI=-0.24 to -0.02; P = 0.02), with inconsistent sensitivity analyses. Additionally, No other causal associations were found.
conclusionOur study indicates that SHBG is a protective factor for MetS, potentially delaying its onset and progression through improvements in HBP and TG. Furthermore, T and E2 may improve TG levels, with T also reducing WC levels. Importantly, our study provides new insights for the prevention and treatment of MetS.
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