Evidence map›Paper›PMID 40394636›Full record

ArticleDiabetology & metabolic syndrome2025

Unraveling the causal pathway between phosphatidylinositol, metabolites, and metabolic syndrome: a Mendelian randomization study.

YueGuang Yang, YanLing Ma, Ming Li, YuBo Han, Li Liu

Abstract read
In one paragraph

Article in Diabetology & metabolic syndrome, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

YueGuang YangHeilongjiang University of Chinese Medicine;, Heilongjiang, P.R. China.
YanLing MaHeilongjiang University of Chinese Medicine;, Heilongjiang, P.R. China.
Ming LiHeilongjiang University of Chinese Medicine;, Heilongjiang, P.R. China.
YuBo HanThe First Department of Cardiovascular, First Affiliated Hospital, Heilongjiang University of Chinese Medicine, 26 Heping Road, Xiangfang, Harbin, Heilongjiang, 150040, P.R. China. hanyb1989@163.com.
Li LiuThe First Department of Cardiovascular, First Affiliated Hospital, Heilongjiang University of Chinese Medicine, 26 Heping Road, Xiangfang, Harbin, Heilongjiang, 150040, P.R. China. liliu429@163.com.

Funding

the Graduate Innovative Research Program of Heilongjiang University of Traditional Chinese Medicine 2024yjscx007the National Natural Science Foundation of China 8207150463, 8227152422, 8220153214
6 · The paper itself

Abstract

introductionObservational studies have increasingly acknowledged the influence of Phosphatidylinositol (PI) on metabolic syndrome (MetS). Nevertheless, the causal association between PI and MetS remains unclear due to the presence of confounding factors and the potential for reverse causation in observational settings. This study seeks to clarify the causal link between PI and MetS while investigating the role of mediating metabolites.

methodsA two-sample Mendelian randomization (MR) analysis was performed to examine the association between PI and MetS, utilizing aggregated data from genome-wide association studies (GWAS). Additionally, a two-step MR approach was applied to quantify the mediation effect of metabolites on the PI-MetS relationship. The inverse variance weighted (IVW) method served as the primary analytical approach, complemented by various sensitivity analyses employing alternative techniques.

resultsA significant positive association was found between genetically predicted PI and a 17% increased risk of MetS. Genetically predicted metabolites, including 4-cholesten-3-one (IVW: OR 1.264, 95% CI 1.076-1.483, p = 0.004), N-acetylalliin (IVW: OR 1.189, 95% CI 1.008-1.402, p = 0.040), and the Adenosine 5'-diphosphate to 5-oxoproline ratio (IVW: OR 1.191, 95% CI 1.045-1.357, p = 0.009), were each significantly associated with an increased risks of MetS, accounting for 14.50, 11.41%, 11.87% and % of the total effect, respectively. Notably, the Retinol to oleoyl-linoleoyl-glycerol ratio (IVW: OR 0.643, 95% CI 0.466-0.887, p = 0.007) mediated 62.6% of the effect, highlighting its pivotal role in the causal pathway linking PI to MetS. Moreover, 1-palmitoyl-2-dihomo-linolenoyl-GPC (IVW: OR 0.865, 95% CI 0.752-0.995, p = 0.042) and the Creatine to carnitine ratio (IVW: OR 0.853, 95% CI 0.740-0.983, p = 0.028) were associated with a reduced risk of MetS, demonstrating inhibitory effects within their respective pathways that accounted to 35.03% and 8.45% reductions in risk, respectively.

conclusionsOur MR analysis demonstrated a positive association between PI and an increased risk of MetS. Furthermore, the metabolite-mediated PI significantly influenced MetS risk. These findings may offer valuable insights into the pathogenesis of MetS and inform future clinical research.

Indexed as

Mendelian randomizationMetabolic syndromeMetabolitePhosphatidylinositol

Identifiers

PMID40394636
PMCPMC12090523

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