Persistent Hyperglycemia and Insulin Resistance With the Risk of Worsening Cardiac Damage in Adolescents: A 7-Year Longitudinal Study of the ALSPAC Birth Cohort

IF 14.8 1区医学 Q1 ENDOCRINOLOGY & METABOLISM

Diabetes Care Pub Date : 2025-05-07 DOI:10.2337/dc24-2459

Andrew O. Agbaje, Justin P. Zachariah, Alan R. Barker, Craig A. Williams, Dimitris Vlachopoulos, Christoph Saner, Tomi-Pekka Tuomainen

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引用次数: 0

Abstract

OBJECTIVE Insulin resistance (IR) and dysglycemia can induce cardiac remodeling in adulthood, but little evidence exists with respect to cardiac remodeling in youth with and without evidence of new-onset glucose metabolic alterations. This study investigated whether changes in metabolic status from adolescence to young adulthood are associated with the risk of progressive cardiac remodeling and examined potential mechanistic pathways. RESEARCH DESIGN AND METHODS From the Avon Longitudinal Study of Parents and Children (ALSPAC), U.K. cohort, 1,595 adolescents, mean (SD) age 17.7 (0.4) years, who had data on fasting plasma glucose and insulin levels, and echocardiography left ventricular (LV) mass indexed for height raised to the power of 2.7 (LVMI2.7) and in whom these factors repeatedly were measured at a clinic visit when they were aged 24 years were included. HOMA-IR was computed, hyperglycemia was defined as glucose concentration of ≥5.6 mmol/L and ≥6.1 mmol/L, and LV hypertrophy was defined as LVMI2.7 ≥51g/m2.7. RESULTS The prevalence of LV hypertrophy increased from 2.4% at baseline to 7.1% at follow-up. Each unit increase of glucose (β = 0.37 g/m2.7 [95% CI 0.23–0.52]; P < 0.001) and HOMA-IR (1.10 g/m2.7 [0.63–1.57]; P < 0.001) was independently associated with increased LVMI2.7 over 7 years. Persistent hyperglycemia of 5.6 mmol/L and 6.1 mmol/L was associated with higher odds (odds ratio [OR] 1.46 [95% CI 1.35–1.47], P < 0.001; and 3.10 [95% CI 1.19–8.08], P = 0.021, respectively) of worsening LV hypertrophy over 7 years. Increased fat mass (62% mediation) significantly mediated the association of increased HOMA-IR with increased LVMI2.7. CONCLUSIONS Persistent adolescent hyperglycemia and worsening IR were associated with the risk of worsening structural and functional cardiac damage, and these were largely explained by increased fat mass.

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青少年持续高血糖和胰岛素抵抗与心脏损伤恶化的风险：一项对ALSPAC出生队列的7年纵向研究

目的胰岛素抵抗（IR）和血糖异常可诱导成年期心脏重构，但很少有证据表明有或没有新发糖代谢改变的青年期心脏重构。本研究调查了从青春期到青年期的代谢状态变化是否与进行性心脏重构的风险相关，并研究了潜在的机制途径。研究设计和方法来自英国雅芳父母与儿童纵向研究（ALSPAC）， 1595名青少年，平均（SD）年龄17.7（0.4）岁，他们有空腹血糖和胰岛素水平的数据，超声心动图左心室（LV）质量指数升高到2.7 (LVMI2.7)，这些因素在他们24岁时在诊所就诊时反复测量。计算HOMA-IR，葡萄糖浓度≥5.6 mmol/L和≥6.1 mmol/L定义为高血糖，LVMI2.7≥51g/m2.7定义为左室肥大。结果左室肥厚的发生率从基线时的2.4%上升到随访时的7.1%。葡萄糖每单位增加(β = 0.37 g/m2.7 [95% CI 0.23-0.52]；P, lt;0.001)和HOMA-IR (1.10 g/m2.7 [0.63-1.57]；P, lt;0.001)与7年内LVMI2.7升高独立相关。5.6 mmol/L和6.1 mmol/L的持续高血糖与较高的比值相关(比值比[OR] 1.46 [95% CI 1.35-1.47], P &；0.001;和3.10 [95% CI 1.19-8.08], P = 0.021，分别)在7年内左室肥厚加重。脂肪量增加（62%介导）显著介导HOMA-IR升高与LVMI2.7升高的关联。结论：青少年持续高血糖和IR恶化与心脏结构和功能损伤恶化的风险相关，这在很大程度上可以用脂肪量增加来解释。

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来源期刊

Diabetes Care 医学-内分泌学与代谢

CiteScore

27.80

自引率

4.90%

发文量

449

审稿时长

1 months

期刊介绍： The journal's overarching mission can be captured by the simple word "Care," reflecting its commitment to enhancing patient well-being. Diabetes Care aims to support better patient care by addressing the comprehensive needs of healthcare professionals dedicated to managing diabetes. Diabetes Care serves as a valuable resource for healthcare practitioners, aiming to advance knowledge, foster research, and improve diabetes management. The journal publishes original research across various categories, including Clinical Care, Education, Nutrition, Psychosocial Research, Epidemiology, Health Services Research, Emerging Treatments and Technologies, Pathophysiology, Complications, and Cardiovascular and Metabolic Risk. Additionally, Diabetes Care features ADA statements, consensus reports, review articles, letters to the editor, and health/medical news, appealing to a diverse audience of physicians, researchers, psychologists, educators, and other healthcare professionals.