ArticleCardiovascular diabetology2024
Causal associations between insulin and Lp(a) levels in Caucasian population: a Mendelian randomization study.
Article in Cardiovascular diabetology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed.
- The Implications of Lipoprotein(a) in MASLD.Current cardiology reports · 2026Review
- Sex- and menopause-specific inverse associations between metabolic dysfunction-associated steatotic liver disease and serum lipoprotein(a) concentrations: evidence from SHIP and UK Biobank.Cardiovascular diabetology · 2026Article
- Lipoprotein(a) levels in Finnish adults: distribution and associations with other cardiovascular risk factors and their awareness and control.Lipids in health and disease · 2026Article
- Distribution of Lipoprotein(a) Levels and Clinical Associations in a Lebanese Adult Population: A Retrospective Observational Study.Journal of clinical medicine · 2026Article
- Lp(a) levels and ischemic stroke recurrence in type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2025Article
- Diabetes Mellitus and Lipoprotein(a): A Determinant Interaction in Micro- and Macrovascular Damage.International journal of molecular sciences · 2025Review
- Effect of changes in the triglyceride-glucose index on atherogenic lipid profiles in coronary artery disease patients receiving lipid-lowering therapy: a prospective cohort study.Cardiovascular diabetology · 2025Article
- Association between lipoprotein(a) and atherosclerosis with different diabetic status: a cross-sectional study in a Chinese population.Cardiovascular diagnosis and therapy · 2025Article
- 2024: The year in cardiovascular disease - the year of lipoprotein(a). Research advances and new findings.Archives of medical science : AMS · 2025Article
- Lipoprotein(a) and the atherosclerotic burden - Should we wait for clinical trial evidence before taking action?Atherosclerosis plus · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNumerous observational studies have demonstrated that circulating lipoprotein(a) [Lp(a)] might be inversely related to the risk of type 2 diabetes (T2D). However, recent Mendelian randomization (MR) studies do not consistently support this association. The results of in vitro research suggest that high insulin concentrations can suppress Lp(a) levels by affecting apolipoprotein(a) [apo(a)] synthesis. This study aimed to identify the relationship between genetically predicted insulin concentrations and Lp(a) levels, which may partly explain the associations between low Lp(a) levels and increased risk of T2D.
methodsIndependent genetic variants strongly associated with fasting insulin levels were identified from meta-analyses of genome-wide association studies in European populations (GWASs) (N = 151,013). Summary level data for Lp(a) in the population of European ancestry were acquired from a GWAS in the UK Biobank (N = 361,194). The inverse-variance weighted (IVW) method approach was applied to perform two-sample summary-level MR. Robust methods for sensitivity analysis were utilized, such as MR‒Egger, the weighted median (WME) method, MR pleiotropy residual sum and outlier (MR-PRESSO), leave-one-out analysis, and MR Steiger.
resultsGenetically predicted fasting insulin levels were negatively associated with Lp(a) levels (β = - 0.15, SE = 0.05, P = 0.003). The sensitivity analysis revealed that WME (β = - 0.26, SE = 0.07, P = 0.0002), but not MR‒Egger (β = - 0.22, SE = 0.13, P = 0.11), supported a causal relationship between genetically predisposed insulin levels and Lp(a).
conclusionOur MR study provides robust evidence supporting the association between genetically predicted increased insulin concentrations and decreased concentrations of Lp(a). These findings suggest that hyperinsulinaemia, which typically accompanies T2D, can partially explain the inverse relationship between low Lp(a) concentrations and an increased risk of T2D.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.