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一项随机的饮食诱导体重减轻干预可降低血浆补体 C3:可能对血管内皮功能障碍有影响。

A randomized diet-induced weight-loss intervention reduces plasma complement C3: Possible implication for endothelial dysfunction.

机构信息

Department of Internal Medicine, CARIM School for Cardiovascular Diseases, Maastricht University and Medical Center, Maastricht, The Netherlands.

Top Institute of Food and Nutrition, Wageningen, The Netherlands.

出版信息

Obesity (Silver Spring). 2022 Jul;30(7):1401-1410. doi: 10.1002/oby.23467.

DOI:10.1002/oby.23467
PMID:35785477
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9545581/
Abstract

OBJECTIVE

Complement C3 and other components of the alternative pathway are higher in individuals with obesity. Moreover, C3 has been identified as a risk factor for cardiovascular disease. This study investigated whether, and how, a weight-loss intervention reduced plasma C3, activated C3 (C3a), and factor D and explored potential biological effects of such a reduction.

METHODS

The study measured plasma C3, C3a, and factor D by ELISA and measured visceral adipose tissue, subcutaneous adipose tissue, and intrahepatic lipid by magnetic resonance imaging in lean men (n = 25) and men with abdominal obesity (n = 52). The men with obesity were randomized to habitual diet or an 8-week dietary weight-loss intervention.

RESULTS

The intervention significantly reduced C3 (-0.15 g/L [95% CI: -0.23 to -0.07]), but not C3a or factor D. The C3 reduction was mainly explained by reduction in visceral adipose tissue but not subcutaneous adipose tissue or intrahepatic lipid. This reduction in C3 explained a part of the weight-loss-induced improvement of markers of endothelial dysfunction, particularly the reduction in soluble endothelial selectin and soluble intercellular adhesion molecule.

CONCLUSIONS

Diet-induced weight loss in men with abdominal obesity could be a way to lower plasma C3 and thereby improve endothelial dysfunction. C3 reduction may be part of the mechanism via which diet-induced weight loss could ameliorate the risk of cardiovascular disease in men with abdominal obesity.

摘要

目的

肥胖个体的补体 C3 和替代途径的其他成分较高。此外,C3 已被确定为心血管疾病的危险因素。本研究旨在探讨减肥干预是否以及如何降低血浆 C3、活化 C3(C3a)和因子 D,并探讨这种降低的潜在生物学效应。

方法

该研究通过 ELISA 测量了血浆 C3、C3a 和因子 D,并通过磁共振成像测量了瘦男性(n=25)和腹型肥胖男性(n=52)的内脏脂肪组织、皮下脂肪组织和肝内脂质。肥胖男性被随机分为习惯性饮食或 8 周饮食减肥干预。

结果

干预显著降低了 C3(-0.15 g/L [95% CI:-0.23 至 -0.07]),但 C3a 或因子 D 没有降低。C3 的减少主要归因于内脏脂肪组织的减少,而不是皮下脂肪组织或肝内脂质。C3 的减少解释了内皮功能障碍标志物改善的一部分,特别是可溶性内皮选择素和可溶性细胞间黏附分子的减少。

结论

男性腹型肥胖的饮食诱导体重减轻可能是降低血浆 C3 的一种方法,从而改善内皮功能障碍。C3 的减少可能是饮食诱导的体重减轻改善腹型肥胖男性心血管疾病风险的机制之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/048d/9545581/3c48b635926c/OBY-30-1401-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/048d/9545581/3c48b635926c/OBY-30-1401-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/048d/9545581/3c48b635926c/OBY-30-1401-g001.jpg

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