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与血浆黄嘌呤氧化还原酶活性相关的胰岛素抵抗,独立于内脏脂肪和脂联素水平:MedCity21健康检查登记处。

Insulin Resistance Associated with Plasma Xanthine Oxidoreductase Activity Independent of Visceral Adiposity and Adiponectin Level: MedCity21 Health Examination Registry.

作者信息

Kurajoh Masafumi, Fukumoto Shinya, Murase Takayo, Nakamura Takashi, Ishihara Takuma, Go Hirofumi, Yamamoto Kouji, Nakatani Shinya, Tsuda Akihiro, Morioka Tomoaki, Mori Katsuhito, Imanishi Yasuo, Inaba Masaaki, Emoto Masanori

机构信息

Department of Metabolism, Endocrinology, and Molecular Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan.

Department of Premier Preventive Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan.

出版信息

Int J Endocrinol. 2019 Dec 30;2019:1762161. doi: 10.1155/2019/1762161. eCollection 2019.

DOI:10.1155/2019/1762161
PMID:32082372
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7012256/
Abstract

BACKGROUND

Higher levels of uric acid production have been reported in individuals with visceral fat obesity, and obesity is known to enhance xanthine oxidoreductase (XOR) activity, although the precise mechanism remains unclear. We investigated the associations of visceral fat area (VFA), serum adiponectin level, and insulin resistance with plasma XOR activity using our novel highly sensitive assay based on [C,N] xanthine and liquid chromatography/triple quadrupole mass spectrometry.

METHODS

This cross-sectional study included 193 subjects (92 males and 101 females) registered in the MedCity21 health examination registry. Plasma XOR activity, serum adiponectin level, and VFA obtained by computed tomography were measured, and insulin resistance was determined based on the homeostasis model assessment (HOMA-IR) index.

RESULTS

The mean values for VFA, log HOMA-IR, and log plasma XOR activity were 76.8 ± 45.8 cm, 0.14 ± 0.30, and 1.50 ± 0.44 pmol/h/mL, respectively. Multiple regression analysis showed that HOMA-IR was significantly (=0.020) associated with plasma XOR activity independent of other factors, including VFA and adiponectin level, as well as age, sex, alcohol drinking habit, smoking habit, alanine transaminase, HbA1c, and eGFR. The " - IR" interaction was not significant (=0.020) associated with plasma XOR activity independent of other factors, including VFA and adiponectin level, as well as age, sex, alcohol drinking habit, smoking habit, alanine transaminase, HbA1c, and eGFR. The ".

CONCLUSIONS

Our results indicate that insulin resistance is associated with plasma XOR activity and that relationship is independent of visceral adiposity and adiponectin level, suggesting that the development of insulin resistance resulting from increased visceral adiposity and/or reduced serum adiponectin contributes to increased uric acid production by stimulating XOR activity.

摘要

背景

据报道,内脏脂肪型肥胖个体的尿酸生成水平较高,且已知肥胖会增强黄嘌呤氧化还原酶(XOR)活性,但其确切机制仍不清楚。我们使用基于[C,N]黄嘌呤和液相色谱/三重四极杆质谱的新型高灵敏度检测方法,研究了内脏脂肪面积(VFA)、血清脂联素水平和胰岛素抵抗与血浆XOR活性之间的关联。

方法

这项横断面研究纳入了MedCity21健康检查登记处登记的193名受试者(92名男性和101名女性)。测量了血浆XOR活性、血清脂联素水平以及通过计算机断层扫描获得的VFA,并根据稳态模型评估(HOMA-IR)指数确定胰岛素抵抗。

结果

VFA、log HOMA-IR和log血浆XOR活性的平均值分别为76.8±45.8 cm、0.14±0.30和1.50±0.44 pmol/h/mL。多元回归分析表明,HOMA-IR与血浆XOR活性显著相关(=0.020),独立于其他因素,包括VFA、脂联素水平以及年龄、性别、饮酒习惯、吸烟习惯、丙氨酸转氨酶、糖化血红蛋白和估算肾小球滤过率。“-IR”交互作用与血浆XOR活性无显著关联(=0.020),独立于其他因素,包括VFA、脂联素水平以及年龄、性别、饮酒习惯、吸烟习惯、丙氨酸转氨酶、糖化血红蛋白和估算肾小球滤过率。

结论

我们的结果表明,胰岛素抵抗与血浆XOR活性相关,且这种关系独立于内脏脂肪过多和脂联素水平,提示内脏脂肪过多增加和/或血清脂联素减少导致的胰岛素抵抗的发展,通过刺激XOR活性促进尿酸生成增加。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/615d/7012256/94db1f901ef4/IJE2019-1762161.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/615d/7012256/6b840d17a7c0/IJE2019-1762161.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/615d/7012256/287b2df7680c/IJE2019-1762161.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/615d/7012256/1ec635c0f624/IJE2019-1762161.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/615d/7012256/94db1f901ef4/IJE2019-1762161.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/615d/7012256/6b840d17a7c0/IJE2019-1762161.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/615d/7012256/287b2df7680c/IJE2019-1762161.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/615d/7012256/1ec635c0f624/IJE2019-1762161.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/615d/7012256/94db1f901ef4/IJE2019-1762161.004.jpg

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