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急性胰腺炎发作后腹部肥胖和胰岛素抵抗。

Abdominal obesity and insulin resistance after an episode of acute pancreatitis.

机构信息

School of Medicine, University of Auckland, Auckland, New Zealand.

Department of Statistics, University of Auckland, Auckland, New Zealand.

出版信息

Dig Liver Dis. 2018 Oct;50(10):1081-1087. doi: 10.1016/j.dld.2018.04.023. Epub 2018 May 1.

Abstract

BACKGROUND

Emerging evidence indicates that individuals after an episode of acute pancreatitis (AP) are at an increased risk of developing metabolic derangements. While the link between general obesity and insulin resistance (IR) is well established, only a few studies have investigated the association between abdominal obesity and IR. The aim of this study was to investigate the associations between abdominal obesity and several indices of IR in individuals after an episode of AP.

METHODS

Patients were eligible for this cross-sectional study if they were previously admitted with a primary diagnosis of AP based on the recent international guidelines. Fasting venous bloods were collected to measure glucose, insulin, free fatty acids, glycerol, adiponectin (AD), omentin (OM), and vaspin (VAS). The IR indices - HOMA-IR, Adipo-IR, insulin*glycerol (IG) index, HOMA-AD, HOMA-OM, and HOMA-VAS were calculated. Modified Poisson regression was conducted, with statistical model adjusting for patient-, metabolic-, and pancreatitis-related risk factors. Areas under ROC curve were calculated and Bland-Altman plots were created.

RESULTS

Of the 92 individuals recruited, 41 had abdominal obesity. HOMA-IR, IG index, HOMA-OM, and HOMA-VAS were significantly associated with abdominal obesity, both in unadjusted and adjusted models. Area under ROC curves for HOMA-IR, IG index, HOMA-OM, and HOMA-VAS were 0.698, 0.695, 0.756, and 0.735, respectively. There was a good agreement between observed HOMA-IR values and values obtained from HOMA-OM (P = 0.733) and HOMA-VAS (P = 0.595).

CONCLUSION

Individuals with abdominal obesity after AP have a significantly higher IR, independent of diabetes and other covariates. Visceral adipose tissue specific adipokines, omentin and vaspin, hold promise for future clinical investigation of tissue-specific IR.

摘要

背景

新出现的证据表明,急性胰腺炎(AP)发作后,个体发生代谢紊乱的风险增加。虽然一般肥胖与胰岛素抵抗(IR)之间的联系已得到充分证实,但只有少数研究调查了腹部肥胖与 IR 之间的关系。本研究旨在探讨 AP 发作后个体腹部肥胖与几种 IR 指标之间的关系。

方法

如果患者符合以下条件,则有资格参加本横断面研究:根据最近的国际指南,之前因原发性 AP 住院。采集空腹静脉血以测量血糖、胰岛素、游离脂肪酸、甘油、脂联素(AD)、网膜素(OM)和内脂素(VAS)。计算 IR 指数 - HOMA-IR、Adipo-IR、胰岛素*甘油(IG)指数、HOMA-AD、HOMA-OM 和 HOMA-VAS。使用调整了患者、代谢和胰腺炎相关危险因素的统计模型进行修正泊松回归。计算 ROC 曲线下面积并绘制 Bland-Altman 图。

结果

在招募的 92 名患者中,有 41 名患有腹部肥胖。在未调整和调整后的模型中,HOMA-IR、IG 指数、HOMA-OM 和 HOMA-VAS 均与腹部肥胖显著相关。HOMA-IR、IG 指数、HOMA-OM 和 HOMA-VAS 的 ROC 曲线下面积分别为 0.698、0.695、0.756 和 0.735。HOMA-IR 值与从 HOMA-OM(P=0.733)和 HOMA-VAS(P=0.595)获得的值之间存在良好的一致性。

结论

AP 后腹部肥胖的个体存在明显更高的 IR,独立于糖尿病和其他协变量。内脏脂肪组织特异性脂肪因子,网膜素和内脂素,有望为未来组织特异性 IR 的临床研究提供新的方向。

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