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肾周脂肪组织堆积与左心室肥厚的关联及胰岛素抵抗的中介作用:一项涉及1112例2型糖尿病患者的横断面研究。

The association of perirenal adipose tissue accumulation with left ventricular hypertrophy and the mediating role of insulin resistance: a cross-sectional study involving 1112 individuals with type 2 diabetes mellitus.

作者信息

Wang Wei, Chen Yang, Qiu Xiu Ping, Guo Xiu Li

机构信息

Department of Endocrinology, Longyan First Affiliated Hospital of Fujian Medical University, Longyan, Fujian, China.

出版信息

Front Endocrinol (Lausanne). 2025 Jan 9;15:1465577. doi: 10.3389/fendo.2024.1465577. eCollection 2024.

DOI:10.3389/fendo.2024.1465577
PMID:39850485
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11754053/
Abstract

OBJECTIVE

Recent studies have underscored the metabolic and cardiovascular regulatory capacity of perirenal adipose tissue (PAT), implicating its potential involvement in the pathogenesis of left ventricular hypertrophy (LVH). This investigation aims to assess the relationship between increased PAT mass and LVH, while also examining the potential mediating role of insulin resistance in this relationship among individuals with type 2 diabetes mellitus (T2DM).

METHOD

1112 individuals with T2DM were prospectively recruited for this study. Perirenal fat thickness (PrFT), measured using unenhanced abdominal CT, served as a measure of PAT mass. The triglyceride to high-density lipoprotein cholesterol ratio (TG/HDL-c) was computed to assess insulin resistance. LVH was identified as left ventricular mass index (LVMI) >115 g/m² in men or LVMI >95 g/m² in women. The correlations of LVH risk with PrFT and TG/HDL-c were analyzed by weighted binomial logistic regression and restricted cubic splines (RCS) analyses. Furthermore, the mediating role of TG/HDL-c in this relationship was explored using the adjusted mediation analysis.

RESULTS

Participants in the LVH group displayed significantly higher PrFT and TG/HDL-c than the non-LVH group ( < 0.001). Adjusting for confounding factors, the LVMI demonstrated a positive correlation with PrFT (=0.262, <0.001) and TG/HDL-c (=0.206, <0.001). PrFT and TG/HDL-c emerged as independent variables for LVH, with odds ratios of 1.33 (95%CI:1.24-1.43, <0.001) and 1.20 (95%CI:1.05-1.36, =0.006), respectively. Each standard deviation increases in PrFT and TG/HDL-c conferred an additional 240% (<0.001) and 41% (=0.006) risk for LVH. A linear correlation of LVH risk with PrFT and TG/HDL-c was observed from RCS analysis ( for nonlinear and overall< 0.001). Moreover, TG/HDL-c mediated 13.4% of the association between PrFT and LVMI, and 8.5% between PrFT and LVH.

CONCLUSION

Increased PAT accumulation contributes to an independent variable for LVH, with insulin resistance acting as a mediating variable in this relationship.

摘要

目的

近期研究强调了肾周脂肪组织(PAT)的代谢和心血管调节能力,提示其可能参与左心室肥厚(LVH)的发病机制。本研究旨在评估PAT质量增加与LVH之间的关系,同时探讨胰岛素抵抗在2型糖尿病(T2DM)患者这一关系中的潜在中介作用。

方法

本研究前瞻性招募了1112例T2DM患者。使用非增强腹部CT测量肾周脂肪厚度(PrFT),作为PAT质量的指标。计算甘油三酯与高密度脂蛋白胆固醇比值(TG/HDL-c)以评估胰岛素抵抗。LVH定义为男性左心室质量指数(LVMI)>115 g/m²或女性LVMI>95 g/m²。通过加权二项逻辑回归和受限立方样条(RCS)分析,分析LVH风险与PrFT和TG/HDL-c的相关性。此外,使用调整后的中介分析探讨TG/HDL-c在这一关系中的中介作用。

结果

LVH组参与者的PrFT和TG/HDL-c显著高于非LVH组(<0.001)。校正混杂因素后,LVMI与PrFT(=0.262,<0.001)和TG/HDL-c(=0.206,<0.001)呈正相关。PrFT和TG/HDL-c是LVH的独立变量,优势比分别为1.33(95%CI:1.24 - 1.43,<0.001)和1.20(95%CI:1.05 - 1.36,=0.006)。PrFT和TG/HDL-c每增加一个标准差,LVH风险分别增加240%(<0.001)和41%(=0.006)。RCS分析观察到LVH风险与PrFT和TG/HDL-c呈线性相关(非线性和总体<0.001)。此外,TG/HDL-c介导了PrFT与LVMI之间13.4%的关联,以及PrFT与LVH之间8.5%的关联。

结论

PAT积累增加是LVH的一个独立变量,胰岛素抵抗在这一关系中起中介变量作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66e4/11754053/ff700382125c/fendo-15-1465577-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66e4/11754053/913a569f3d06/fendo-15-1465577-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66e4/11754053/32895dbe77a8/fendo-15-1465577-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66e4/11754053/ff700382125c/fendo-15-1465577-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66e4/11754053/913a569f3d06/fendo-15-1465577-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66e4/11754053/32895dbe77a8/fendo-15-1465577-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66e4/11754053/d15dd588513f/fendo-15-1465577-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66e4/11754053/ff700382125c/fendo-15-1465577-g004.jpg

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