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超重和肥胖儿童中维生素 D、趋化素与代谢特征之间的关联——初步研究结果。

The link between vitamin D, chemerin and metabolic profile in overweight and obese children - preliminary results.

机构信息

Department of Paediatrics and Endocrinology, Medical University of Warsaw, Warsaw, Poland.

Department of Laboratory Diagnostics and Clinical Immunology of Developmental Age, Medical University of Warsaw, Warsaw, Poland.

出版信息

Front Endocrinol (Lausanne). 2023 Apr 20;14:1143755. doi: 10.3389/fendo.2023.1143755. eCollection 2023.

DOI:10.3389/fendo.2023.1143755
PMID:37152969
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10159269/
Abstract

BACKGROUND

Vitamin D affects adipogenesis, oxidative stress, inflammation, secretion of adipocytokines, lipid metabolism and thermogenesis. Some researchers postulate that those effects could be exerted by the influence of vitamin D on chemerin levels.

AIM OF THE STUDY

We aimed to investigate if there is a link between serum 25-hydroksyvitamin D [25(OH)D], chemerin and metabolic profile in overweight and obese children before and after vitamin D supplementation.

MATERIAL AND METHODS

The prospective study included 65 overweight and obese children aged 9.08-17.5 years and 26 peers as a control. None of the patients in the study group had received vitamin D within the last twelve months before the study.

RESULTS

The study group had lower baseline 25(OH)D (p<0.001) and higher chemerin (p<0.001), triglycerides (TG, p<0.001), triglycerides/high density lipoprotein cholesterol (TG/HDL-C, p<0.001), C-reactive protein (CRP, p<0.05), fasting insulin (p<0.001), Homeostasis Model Assessment - Insulin Resistance (HOMA-IR, p<0.001), alanine aminotransferase (ALT, p<0.001) and uric acid (p<0.001) compared to the control group. Baseline vitamin D was related to fasting insulin (R=-0.29, p=0.021), HOMA-IR (R=-0.30, p=0.016), HDL-C (R=0.29, p=0.020) and uric acid (R=-0.28, p=0.037) in the study group. Baseline chemerin was related to insulin at 30' (R=0.27, p=0.030), 60' (R=0.27, p=0.033), 90' (R=0.26, p=0.037) and 120' (R=0.26, p=0.040) during the oral glucose tolerance test (OGTT) and ALT (R=0.25, p=0.041) in the study group. Correlation between vitamin D and chemerin (R=-0.39, p=0.046) was found only in the control group. After six months of vitamin D supplementation a decrease in CRP (p<0.01), total cholesterol (p<0.05), ALT (p<0.01), glucose at 150' OGTT (p<0.05) was observed. Moreover, we noticed a tendency for negative association between 25(OH)D and chemerin levels (p=0.085). Multivariable backward linear regression models were build using baseline vitamin D, baseline chemerin and six months chemerin as the dependent variables.

CONCLUSIONS

Our study confirmed that vitamin D has positive effect on metabolic profile in overweight and obese children. The relationship between vitamin D and chemerin is not clear, nevertheless we have observed a tendency to decrease chemerin concentrations after improving vitamin D status, even without a significant reduction in body fat mass.

摘要

背景

维生素 D 影响脂肪生成、氧化应激、炎症、脂肪细胞因子的分泌、脂质代谢和产热。一些研究人员假设,这些影响可能是维生素 D 对趋化素水平的影响所致。

目的

我们旨在研究超重和肥胖儿童在补充维生素 D 前后血清 25-羟维生素 D [25(OH)D]、趋化素和代谢特征之间是否存在关联。

材料和方法

前瞻性研究纳入了 65 名年龄在 9.08-17.5 岁的超重和肥胖儿童和 26 名同龄人作为对照组。研究组中没有一名患者在研究前的 12 个月内接受过维生素 D。

结果

与对照组相比,研究组的基础 25(OH)D 水平较低(p<0.001),趋化素(p<0.001)、三酰甘油(TG,p<0.001)、三酰甘油/高密度脂蛋白胆固醇(TG/HDL-C,p<0.001)、C 反应蛋白(CRP,p<0.05)、空腹胰岛素(p<0.001)、稳态模型评估-胰岛素抵抗(HOMA-IR,p<0.001)、丙氨酸氨基转移酶(ALT,p<0.001)和尿酸(p<0.001)水平较高。基础维生素 D 与空腹胰岛素(R=-0.29,p=0.021)、HOMA-IR(R=-0.30,p=0.016)、高密度脂蛋白胆固醇(R=0.29,p=0.020)和尿酸(R=-0.28,p=0.037)呈负相关。基础趋化素与口服葡萄糖耐量试验(OGTT)30'(R=0.27,p=0.030)、60'(R=0.27,p=0.033)、90'(R=0.26,p=0.037)和 120'(R=0.26,p=0.040)时的胰岛素以及 ALT(R=0.25,p=0.041)呈正相关。仅在对照组中发现维生素 D 和趋化素之间存在负相关(R=-0.39,p=0.046)。在接受六个月的维生素 D 补充后,观察到 CRP(p<0.01)、总胆固醇(p<0.05)、ALT(p<0.01)、150'OGTT 时的葡萄糖水平(p<0.05)下降。此外,我们注意到 25(OH)D 和趋化素水平之间存在负相关的趋势(p=0.085)。使用基础维生素 D、基础趋化素和六个月趋化素作为因变量建立了多元向后线性回归模型。

结论

我们的研究证实,维生素 D 对超重和肥胖儿童的代谢特征有积极影响。维生素 D 和趋化素之间的关系尚不清楚,但我们观察到,在改善维生素 D 状态后,趋化素浓度有下降的趋势,即使体脂质量没有显著减少。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94d7/10159269/4580d21d66e9/fendo-14-1143755-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94d7/10159269/1008e7d17d0b/fendo-14-1143755-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94d7/10159269/4d4001ecf25f/fendo-14-1143755-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94d7/10159269/d4bbbcbc3474/fendo-14-1143755-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94d7/10159269/4580d21d66e9/fendo-14-1143755-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94d7/10159269/1008e7d17d0b/fendo-14-1143755-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94d7/10159269/4d4001ecf25f/fendo-14-1143755-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94d7/10159269/d4bbbcbc3474/fendo-14-1143755-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94d7/10159269/4580d21d66e9/fendo-14-1143755-g004.jpg

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